bluuebunny/crossref_metadata_2025 huggingface dataset:
Immune responses during pregnancy. Evidence of suppressor cells for splenic antibody response.
Authors: Suzuki K , Tomasi T B
Published: June 2004

The primary IgM antibody response to sheep erythrocytes in vivo as well as in vitro is markedly decreased in the spleen cells of pregnant mice, compared to age-matched female controls. Decreased antibody synthesis appears to be mediated by nonspecific suppressor cells, because the addition of pregnant spleen cells to the normal spleen cell cultures causes a significant suppression of plaque-forming-cell responses of the normal spleen cells. Suppressor cell activity was not observed in lymph nodes of pregnant mice. At least two populations of pregnant spleen cells were shown to exert a suppressor cell activity; one is T lymphocytes and the other a nylon-adherent cell present in the B-cell-enriched macrophage-depleted fraction. Pregnant spleen cells cultured in vitro were shown to secrete a soluble suppressive factor(s) into the supernatant medium.
Association of alkaline-phosphatase-positive reticulum cells in bone marrow with granulocytic precursors.
Authors: Westen H , Bainton D F
Published: June 2004

In the bone marrow, an elaborate stroma forms the structural basis of the hemopoietic microenvironment. In this study, two different types of stromal cells were identified with certainty on tissue sections of intact bone marrow of rats and mice using light and electron microscopic histochemistry: (a) a fibroblast-type of reticulum cell which is characterized by having alkaline phosphatase associated with its plasma membrane. We refer to this cell as the alkaline-phosphatase-positive reticulum cell (Al-RC). It is closely associated with granulocytic precursors, particularly myeloblasts and neutrophilic promyelocytes. These reticulum cells may be found throughout the marrow but are concentrated near the endosteum. (b) a macrophage-type of reticulum cell which is characterized by its abundance of lysosomal acid phosphatase and is mainly associated with erythroid precursors (as observed by others). In contrast to the above-mentioned cell type, this latter cell was found to be distributed uniformly throughout the marrow. We speculate that the Al-RC are mesenchymal stromal cells necessary for granulocytic differentiation in bone marrow.
Major histocompatibility complex-restricted antibody reactivity mainly, but not exclusively, directed against cells from male donors.
Authors: van Leeuwen A , Goulmy E , van Rood J J
Published: June 2004

An IgM antibody, present in the serum of a female patient with aplastic anemia, is described that reacted in a modified complement-dependent cytotoxicity test with a subset of the B cells from HLA-A2-positive, but not HLA-A2-negative males. With the exception of two HLA-A2 positive females, the antibody did not react with other cells from either HLA-A2-positive or HLA-2-negative females. The cells of one of these and from HLA-A2-positive males were able to absorb the antibody from the serum. Cells from other donors were unable to absorb the antibodies. The mononuclear cells of the same patient were cytolytic in cell-mediated lympholysis (CML) for phytohemagglutinin blasts from all HLA-A2-positive males and one of the females reacting with antibody, but not with blasts from HLA-A2-negative males and all other females. Thus, the results obtained with the antibody in the complement-dependent cytotoxicity test showed an almost perfect correlation with cytolysis in CML tests. These results suggest that the IgM antibody may be the first example with major histocompatibility complex restriction. Because the antibody reacted with the cells from two female donors, the restricting determinant is not, in all probability, the H-Y determinant.
Binding of purified, soluble major histocompatibility complex polypeptide chains onto isolated T-cell receptors. I. Reactivity against allo- and self-determinants.
Authors: Binz H , Frischknecht H , Mercolli C , Dunst S , Wigzell H
Published: June 2004

In this study, we tried to get information about the fine antigen-binding ability of purified, soluble, idiotype-positive T-cell receptor molecules. Lewis anti-DA T-cell receptors were purified from normal Lewis serum by the use of anti-idiotypic immunosorbent and sodium dodecyl sulfate-polyacrylamide gel, and were coupled to cyanogen bromide-activated Sepharose 4B. In parallel, Lewis anti-DA, Lewis anti-BN, and DA anti-Lewis alloantibody immunosorbents were prepared. The major Ag-B chain (44,000 daltons) and the two polypeptide chains (34,000 and 27,000 daltons) of Ia were purified from Lewis, DA, and BN lymphocytes and absorbent on the above-mentioned immunosorbents. We found that the major Ag-B chain as well as the two Ia chains were bound to the alloantibody columns if they were derived from the corresponding allogeneic strain. No retaining ability for self-major histocompatibility complex (MHC) or third-party MHC chains was noted with the alloantibody immunosorbents. When using immunosorbents made up of idiotypic T-cell receptors, only two MHC polypeptides of the relevant allo-MHC type were retained, namely, the Ag-B and the heavy Ia chains. No detectable activity was observed when testing the same column for reactivity against third-party MHC polypeptide chains. However, the Lewis anti-DA T-cell receptors could be shown to display weak, but significant, reactivity toward one Lewis MHC polypeptide chain, that is, the heavy chain of Ia type.
The specific binding of Listeria monocytogenes-immune T lymphocytes to macrophages. I. Quantitation and role of H-2 gene products.
Authors: Ziegler K , Unanue E R
Published: June 2004

A system was developed to study the binding of Listeria monocytogenes-specific T cells to L. monocytogenes-pulsed macrophages as an analogue of the initial phase of T-cell activation: antigen recognition. Specific binding, demonstrable after a brief (1 h) contact, was quantitated by the depletion of L. monocytogenes-specific T-cell activity in the cells nonadherent to L. monocytogenes-pulsed macrophage monolayers. L. monocytogenes-specific T-cell function was measured by its ability to activate L. monocytogenes-pulsed macrophages, both to secrete a protein mitogenic for thymocytes and to effect nonspecific tumoricidal activity. These manifestations of T-cell function are known to be regulated by products of I region of the H-2 gene complex. Studies designed to determine the role of H-2 gene products in specific T-cell-macrophage binding have revealed the following. T cells bind specifically to syngeneic macrophages and poorly to allogeneic macrophages. The binding ability appears to map to the K end of the H-2 gene complex (K through I-E). At least two distinct populations of B6AF1 T cells with binding avidity for L. monocytogenes presented on parental macrophages can be identified. Finally, the binding of a given parental-reactive B6AF1 T-cell clone can be specifically inhibited by pretreatment of the antigen-pulsed B6AF1 binding macrophage with anti-H-2 (anti-Ia) antibodies reactive with the appropriate parental haplotype. These results strongly suggest that H-2 gene products play a direct role in mediating the specific binding of T cells to macrophages and imply that the antigen-dependent physical interaction between T cells and macrophages is the initial, and determining, event in some forms of H-2 gene control of immune reactivity.
Experimental IgA nephropathy.
Authors: Rifai A , Small P A , Teague P O , Ayoub E M
Published: June 2004

An animal model for IgA immune complex nephritis was developed. IgA immune complexes formed in vitro with an IgA anti-dinitrophenyl (DNP) derived from MOPC-315 plasmacytoma, and dinitrophenylated bovine serum albumin (DNP-BSA) produced mild focal glomerulonephritis in mice. Similar, but more severe pathological changes were produced with complexes formed in vivo either in normal mice or MOPC-315 tumor-bearing mice. In contrast to the focal nature of the PAS-positive glomerular lesions observed by light microscopy, immunofluorescent examination revealed IgA deposits in all glomeruli. This discrepancy between immunofluorescent and histopathologic findings as well as the distribution of the immune complexes within the affected glomeruli, are some of the features which bear resemblance between this experimental model and human IgA nephropathy. Fixation of complements by DNP-BSA-IgA immune complexes, formed in vitro or in vivo, was shown to occur in the glomeruli of mice with IgA immune complex nephropathy. The pattern of C3 glomerular deposits was similar to that of IgA. However, complement proved to be nonessential for complex deposition. This conclusion is based on the observation that decomplemented mice, although showing no deposition of C3 in their glomerulus, developed glomerular immunohistological changes similar to those observed in experimental mice that were not decomplemented. Polymeric IgA was observed to be critical for renal deposition of complexes and induction of nephritic histological changes. In contrast, monomeric IgA immune complexes failed to produce glomerular deposits. This finding raises the possibility that secretory IgA, which is predominantly polymeric, may play a role in human IgA-associated glomerulonephritis.
Viral specificity of H-2-restricted T killer cells directed against syngeneic tumors induced by Gross, Friend, or Rauscher leukemia virus.
Authors: Plata F , Lilly F
Published: June 2004

Cytolytic T lymphocytes (CTL) were generated against murine tumors induced by Gross, Friend, or Rauscher leukemia virus (LV) in syngeneic mixed leukocyte-tumor cell cultures. Analogous to the patterns of specificity observed with antibodies to LV-induced cell surface antigens, CTL could be classified into two major groups of specificity. Tumor cells induced by Friend, Moloney, or Rauscher virus and positive for the FMR antigen were killed by syngeneic CTL immune to any one of these three LV; the same CTL, however, were incapable of killing syngeneic tumor cells induced by Gross LV. The converse was true for Gross LV-specific CTL: these CTL were specific for syngeneic tumor cells expressing the Gross virus-associated cell-surface antigen (GCSA), and not the FMR antigen. The H-2 specificities of the two groups of LV-immune CTL were also compared, because in both cases, CTL were restricted in their killing activity to H-2-identical tumor target cells. When CTL from single strains of mice were generated against syngeneic FMR- or GCSA-positive tumor cells, differences were observed with respect both to the requirement for the expression of compatible H-2K or H-2D specificities, and to the intensity of the CTL response in congenic mice of the H-2b, H-2d, and H-2k haplotypes.
Tumorigenicity of Indian muntjac diploid cells by the proviral integration of sarcoma gene of a mouse retrovirus.
Authors: Hatanaka M , Klein R
Published: June 2004

The transformed clonal isolates of Indian muntjac diploid cells by a mouse sarcoma virus, 43-2XV, were tested for tumorigenicity in athymic nude mice. In spite of the indistinguishable transformed morphology, the tumorigenicity exhibited four different patterns: (a) no tumor formation; (b) slowly growing regressive tumor formation; (c) rapidly growing regressive tumor formation; and (d) rapidly growing progressive tumor formation. This demonstrates that the same diploid host cells transformed by the same virus reveal variable patterns of tumorigenic expression and some transformed host cells lack the tumorigenicity entirely. The findings that there are at least two chromosomes and four recombinant sites assigned for the proviral integrations of the sarcoma gene into the Indian muntjac gene (M. Hatanaka, R. Klein, R. Kominami, T. Oikawa, H. Okabe, N. Tsuchida, E. C. Connors, and A. Carrano. Transformation of Indian muntjac diploid cells by the proviral integration of sarcoma gene of a mouse retrovirus. Manuscript in preparation.) lead us to propose a hypothesis that variable expressions of tumorigenicity under the neutral background of immune responses, may arise from variable integrations of the sarcoma gene into the host chromosome.
Ontogeny of B cells in CBA/N mice. Evidence for a stage of responsiveness to thymus-independent antigens during development.
Authors: Lindsten T , Andersson B
Published: June 2004

This paper deals with the CBA/N mice, a strain bearing a genetic defect in their B-cell compartment. By using a previously described system we have been able to show that the immature cells of CBA/N mice are functionally indistinguishable from normal immature cells, in that both can be triggered to respond to thymus-independent (TI) antigens, provided they are supplied with helper T cells. When the maturation is completed, CBA/N B cells are unable to respond to TI antigens (like lipopolysaccharide and polyvinyl pyrrolidine) irrespective of the presence of helper T cells, whereas normal mature B cells have grown able to respond without any help. These data allow us to reject the hypothesis that CBA/N mice are arrested at an immature stage and clearly support the idea that they have deviated during development so that only thymus-dependent B cells develop.
B6.C-H-2bm12. A new H-2 mutation in the I region in the mouse.
Authors: McKenzie I F , Morgan G M , Sandrin M S , Michaelides M M , Melvold R W , Kohn H I
Published: June 2004

The B6.C-H-2bm12 mutant is described and evidence is presented for the mutational site occurring in the IA subregion. The mutant is of the gain and loss type as bm12 in equilibrium or formed from C57BL/6 grafts are rejected in 14-16 d. Mapping studies by the gene-complementation method using H-2 recombinant strains place the mutation in the K or IA regions of the H-2 complex and furthermore, the use of this test and the use of other H-2 mutants indicate that H-2Kb is not the site of the mutation, making the IA region the most likely site. Serological analysis with a battery of H-2b, Iab, and other Ia sera, both by cytotoxicity, rosetting, and also by absorption analysis, indicated no alteration in H-2 specificities, particularly in H-2.K33. By contrast, all of the Iab specificities coded for by the IA subregion (Ia.3, 8, 9, 15, and possibly 20) are extensively altered and are either absent or greatly reduced in amount indicating an extensive alteration in the Ia-bearing molecule. The bm12 mutant strongly stimulates the parental C57BL/6 strain in an mixed lymphocyte reaction (MLR), and the reciprocal also occurs, the degree of stimulation being similar to that obtained with K + IA differences originating in another H-2 haplotype and points to the mutation effecting the Lad-1 locus. The presence of an extensive histocompatibility change, a marked alteration in the serologically detected Ia specificities, and a strong MLR, all produced by the one mutation, provides strong evidence for the identity of the Ia-1, Lad-1, and H-2(IA) loci in the IA subregion. The bm12 mutant should be of value in determining the relationship of Ia specificities, Ir genes, and other phenomena effected by the I region.
Inhibition of collagen synthesis by mononuclear cell supernates.
Authors: Jimenez S A , McArthur W , Rosenbloom J
Published: June 2004

Mononuclear cell infiltration and alteration in the connective tissues are prominent features of the inflammatory response in a number of diseases. To determine whether mononuclear cell products can modulate collagen synthesis, human peripheral mononuclear cells from normal donors were isolated by Ficoll-Hypaque gradient centrifugation and then incubated for 48 h with or without phytohemagglutinin. Confluent cultures of normal, human skin fibroblasts were incubated with [14C]proline and various amounts of dialyzed supernates from the mononuclear cell cultures. Labeled, newly synthesized collagen was estimated by [14C]hydroxyproline analysis, collagenase digestion, and chromatography on Agarose A-5m in sodium dodecyl sulfate. The total incorporation of [14C]proline was not significantly affected by addition of the mononuclear cell supernates, but as much as 90% decrease in the synthesis by the fibroblasts of labeled collagen was found relative to controls. Supernates from the phytohemagglutinin-stimulated cultures were more active than those from nonstimulated cells. These results suggest that mononuclear cells can synthesize a factor(s) which can selectively inhibit collagen synthesis.
Interactions between human eosinophils and schistosomula of schistosoma mansoni. II. The mechanism of irreversible eosinophil adherence
Authors: Butterworth AE , Vadas MA , Wassom DL , Dessein A , Hogan M , Sherry B , Gleich GJ , JR David
Published: June 2004

Previous work (1)(1) has shown that normal human eosinophils show a preferential capacity, in comparison with neutrophils, to bind to antibody- coated schistosomula of Schistosoma mansoni. This effect is attributable to a temperature-dependent function of the eosinophil which renders its binding stable and irreversible by aggregated gamma globulin or Staphylococcus aureus protein A. In contrast, the binding of neutrophils is readily reversible by these agents.

It has now been shown that the differences observed between eosinophils and neutrophils is a property of their interaction with living schistosomula. When dead or artificially damaged schistosomula were tested, neutrophils showed a markedly enhanced capacity to adhere, in both the presence and absence of anti-chistosomular serum.

Subsequent experiments were designed to test the hypothesis that the strong, stable binding of eosinophils was attributable to degranulation, with release of granule contents which would then serve as ligands to bind the cell to the organism. First, an enhanced adherence both of eosinophils and of neutrophils could be demonstrated in the presence of eosinophil major basic protein (MBP) or of protamine, a high molecular weight cation. Second, the binding of eosinophils induced by concanavalin A (Con A) was found to differ markedly from that induced by antischistosomular serum. Con A-mediated binding of eosinophils was fully reversible by alpha-methyl-mannoside, was not associated with damage to the organism, and did not lead to degranulation of the cell, as estimated by measuring the release of MBP into the culture supernate. However, induction of degranulation of concanavalin A-bound eosinophils, but not of neutrophils, with the calcium ionophore A23187 converted the reaction into one which was no longer reversible by alpha- methylmannoside and in which damage to the organism now did occur.

These findings support the hypothesis that the stable binding of eosinophils is associated with degranulation, a process which may contribute to the preferential capacity of this cell to mediate antibody-dependent damage to schistosomula.
Expression of endogenous xenotropic retrovirus by methylcholanthrene-induced squamous cell carcinoma of the mouse respiratory tract.
Authors: Ebenstein P , Kinder B , Bankole D O , Richards F F , Armstrong M Y
Published: June 2004

As a model for human lung cancer, squamous cell carcinomas were induced by 3-methylcholanthrene in mouse tracheas which had been explanted to a subcutaneous site. The tumors that developed were examined for both ecotropic and xenotropic infectious murine leukemia virus (MuLV). From all squamous carcinomas--six out of six--a xenotropic MuLV was isolated. From some of the fibrosarcomas that occurred incidentally in our induction system, ecotropic MuLV was isolated. However, in the fibrosarcomas, no xenotropic MuLV at all was found.
Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide.
Authors: Pabst M J , Johnston R B
Published: June 2004

After in vitro exposure to lipopolysaccharide (LPS) or muramyl dipeptide (MDP), cultured resident mouse peritoneal macrophages were primed to display enhanced generation of superoxide anion (O2-) in response to stimulation by phorbol myristate acetate (PMA) or opsonized zymosan. Priming with LPS (1 microgram/ml) produced a sevenfold enhancement of PMA-stimulated O2- generation; priming was detected within 30 min and persisted for at least 4 d. Exposure to MDP (1 muM) primed the macrophages to double their O2- release; the response was first observed after 4 h and persisted for at least 3 d. The priming response was not observed with stereoisomers of MDP, which are inactive as adjuvants. LPS and MDP appeared to work directly on the macrophages rather than indirectly by interacting with adherent lymphocytes: (a) Addition of nonadherent cell populations that contained lymphocytes had no effect on the response. (b) The response was normal with cells from nude mice, which lack mature T lymphocytes. (c) Macrophages from C3H/HeJ mice, whose B lymphocytes fail to respond to LPS, were weak in their response to priming LPS; the addition of normal (C3Heb/FeJ) nonadherent cells had no effect on this weak response. (d) The macrophage-like cell line J774.1 also showed enhanced O2--generating capacity after a 4-h exposure to LPS or MDP. The O2--generating capacity of macrophages primed with LPS in vitro was equivalent to that previously observed with cells elicited in vivo by injection of LPS or activated by infection with Bacille Calmette-Guérin. The data suggest that previous exposure to bacterial products could prime macrophages to respond with increased production of toxic oxygen metabolites on contact with invading microorganisms or tumor cells.
T cells that encounter virus in the complete absence of a particular H-2 antigen are nonresponsive when stimulated again in the context of that H-2 antigen.
Authors: Bennink J R , Doherty P C
Published: June 2004

Immunologically naive BALB/c (H-2d) and C57BL/6J (B6) (H-2b) T-cell populations can, after filtration to remove alloreactive precursor lymphocytes, be induced to respond to vaccinia virus presented in the context of H-2Kk when stimulated in an appropriate recipient. Exposure to vaccinia virus 6 wk previously completely abrogated the capacity of BALB/c T cells to interact with H-2Kk-vaccinia virus. This is also true for negatively selected B6 thoracic duct lymphocytes taken at 14 or 18 d, but not at 6 wk after immunization: the discrepancy is thought to reflect the progressive emergence of new T cells in the latter group. No evidence could be found for the operation of suppression, and the results are considered to indicate that T cells that interact with virus in the absence of the relevant H-2 antigen are tolerized. Whereas stimulation to effector function is H-2 restricted, induction of immune paralysis may be unrestricted. The capacity of T-cell populations to respond to virus presented in the context of allogeneic H-2 determinants thus depends upon previous antigenic experience.
Human cytotoxic T-cell responses to type A and type B influenza viruses can be restricted by different HLA antigens. Implications for HLA polymorphism and genetic regulation.
Authors: Shaw S , Shearer G M , Biddison W E
Published: June 2004

The present study compares human cytotoxic T-cell responses to two closely related viruses (type A and type B influenza) to understand the antigen-specific elements involved in HLA-linked genetic control of cytotoxic T-cell responses. The HLA antigens function as self antigens that are recognized by cytotoxic T cells sensitized against either virus. However, studies in an informative family indicate that in this family, the HLA antigens preferentially recognized in conjunction with type A influenza (A/HK) differ from the HLA antigens preferentially recognized in conjunction with type B influenza (B/HK). Similarly, population studies demonstrate that some (but not all) donors whose T cells recognized A/HK in conjunction with HLA-A2 failed to recognize B/HK in conjunction with HLA-A2. Thus, HLA-linked regulation must operate by a mechanism(s) that is specific both for the self HLA antigen and the viral antigen. Furthermore, these findings indicate that different HLA antigens may facilitate T-cell responses to different pathogens, which would result in an evolutionary advantage for HLA heterozygosity.
Loss of Fc receptor activity after culture of human monocytes on surface-bound immune complexes. Mediation by cyclic nucleotides.
Authors: Ragsdale C G , Arend W P
Published: June 2004

Human monocytes cultured on surface-bound immune complexes exhibited a loss of ability to form rosettes with IgG-sensitized sheep erythrocytes (EA). This loss was not a result of inhibition of Fc receptors by solubilized complexes nor of release of soluble factors by the cells. Loss of EA rosetting was not prevented by culture of monocytes at 4 degrees C, or by treatment with colchicine, cytochalasin B, or local anethetic agents. These results suggested that the loss was not secondary to capping or interiorization of Fc receptors. The results of other studies indicated that the Fc receptors were not damaged by lysosomal enzymes or oxygen radicals. Maintenance of EA rosetting ability of monocytes cultured on surface-bound immune complexes was seen after a 3-h preincubation of the cells in 100 mM 2-deoxy-D-glucose (2dG). A similar preincubation in ATP or in 8-bromoadenosine 3':5'-cyclic monophosphoric acid plus the phosphodiesterase inhibitor methyl isobutyl xanthine led to a partial loss of EA rosetting of cells on plain fibrin and to a partial reversal of the effects of 2dG seen with cells on complexes. We conclude that EA rosetting of monocytes cultured on surface-bound immune complexes is reduced by cyclic nucleotide-mediated effects on Fc receptor number or function.
Biochemical and immunological characterization of the extracellular nucleases of group B streptococci.
Authors: Ferrieri P , Gray E D , Wannamaker L W
Published: June 2004

Nearly all group B streptococcal strains representing the five major serotypes were found to produce extracellular nucleases by screening with an agar-well-diffusion technique in DNA-methyl green agar plates. Three different nucleases have been isolated and partially purified by DEAE-and carboxymethyl-cellulose chromatography. They possessed different mobilities on polyacrylamide gel electrophoresis and different molecular weights. These nucleases, designated I, II, and III, are optimally activated by cations of calcium and manganese and exhibited RNase as well as DNase activity. Despite differences in their physical and biochemical properties, nucleases II and III appear antigenically similar, but distinct from nuclease I. These group B streptococcal nucleases are immunologically different from the nucleases of group A streptococci. Neutralizing activity, probably antibody, to nucleases II and III was found in human sera, and was most prevalent in sera of pregnant women colonized with group B streptococci and in their newborn infants.
I-N: a newly described H-2 I subregion between K and I-A.
Authors: Hayes C E , Bach F H
Published: June 2004

Strong, primary mixed leukocyte culture-proliferative responses in certain K region-incompatible strain combinations led us to consider whether an I region-like locus might exist between K and I-A. Results obtained with an (A. TL X B10.D2)F1 anti-B10.BR serum provided serological evidence for a new locus; B10.T(6R)-absorbed serum retained reactivity on AQR lymphocytes. This finding demonstrates an antigen, Ia.W41, encoded by a locus, Ia-7, within a new I subregion, I-N.
Lymphomagenicity of recombinant mink cell focus-inducing murine leukemia viruses.
Authors: Cloyd M W , Hartley J W , Rowe W P
Published: June 2004

Recombinant mink cell focus-inducing (MCF) murine leukemic viruses, as well as ecotropic and xenotropic viruses, were tested for ability to accelerate or cause development of lymphoma in AKR and other strains of mice. Of the three classes of virus isolated from AKR, only the MCF viruses were able to accelerate development of AKR lymphoma. This fully supports the idea that the MCF viruses are the proximal cause of spontaneous AKR lymphoma. MCF lymphomagenicity was strain specific, however, in that AKR MCF viruses did not induce lymphomas in many murine strains; they were moderately lymphomagenic in C3H/Bi mice and in National Institutes of Health Swiss partially congenic for Akv-1 or Akv-2. In contrast, MCF viruses from nonthymic hematopoietic neoplasms of C3H/Fg, BALB/c, or mice partially congenic for ecotropic virus loci (Akv-1, Akv-2, Fgv-1, C58v-1, and C58v-2) were not able to accelerate or cause lymphomia in AKR or any other mouse strain tested, including some of the strains of origin. MCF lymphomagenicity correlated with thymic origin in the virus and with ability to replicate in the thymus.
Developmental and communicative interrelations of Ly123 and Ly1 cell sets.
Authors: Shen F W , McDougal J S , Bard J , Cort S P
Published: June 2004

To distinguish and define the differentiative and communicative relations of Ly123 and Ly1 cells in generating specific helper-effector (HE) (Ly1:HE) and specific suppression-inducing (SI) (Ly1:SI) cells, these two functional sets were generated from various combinations of congenic genetically marked sets of cortisone-resistant nylon-purified thymocytes (CRNPT) by culture on antigen-primed macrophages (M phi) (the (T-M phi culture system). It was thus shown that Ly1:HE and Ly1:SI cells are produced by differentiation from antecedent Ly123 cells. Ly1:HE and Ly1:SI are separate Ly1 populations; generationof Ly1:HE cells requires the presence of Ly1 cells, whereas the generation of Ly1:SI cells does not. Although the Ly23 CRNPT set, which is included when Ly123 cells are positively selected with Lty-2 antiserum is ruled out as a precursor source of Ly1:SI cells, the possibility of a communicative role for Ly23 cells in generating Ly1:SI cells remains to be investigated. The role of the Ly1 set required for the generation of Ly1:HE cells from CRNPT is communicative, not differential; and it is not a precursor source of Ly1:HE or Ly1:SI cells in the CRNPT population. It remains to be seen whether the use of additional phenotypic markers will distinguish subsets of Ly123 and Ly1 cells engaged in these several functions.
Dichotomy between the induction of suppressor cells and immunologic tolerance by adult thymectomy.
Authors: Borel Y , Kilham L , Kurtz S E , Reinisch C L
Published: June 2004

Adult thymectomy prevents the development of suppressor T cells without impairing the induction of immunologic tolerance to the same antigenic determinant. This finding demonstrates that the cellular mechanisms underlying immune suppression and immune tolerance are different.
Separate cytotoxic T lymphocyte subsets recognize the different H-2 specificities.
Authors: Vazquez A , Néauport-Sautès C , Senik A
Published: June 2004

Using a monolayer adsorption technique, the fine specificity of cytotoxic effector T lymphocytes (CTL) generated against allogeneic or semi-allogeneic H-2 haplotypes was investigated. The results show that: (a) CTL reacting with the private specificity expressed on an H-2.K molecule can be separated from those reacting with the public specificities expressed on the same molecule and (b) the CTL that recognize cross-reacting H-2 determinants (public specificities) can also be separated into several subpopulations. These data support the hypothesis that an allogeneic stimulation induces a large number of independent T cell clones that react with H-2 determinants.
Determinants on surface proteins of Plasmodium knowlesi merozoites common to Plasmodium falciparum schizonts.
Authors: Miller L H , Johnson J G , Schmidt-Ullrich R , Haynes J D , Wallach D F , Carter R
Published: June 2004

In this report and (R. Schmidt-Ullrich, L. H. Miller, and D. F. H. Wallach. Manuscript in preparation.), we have demonstrated that malaria proteins on the surface of merozoites and infected erythrocytes cross-react between at least two primate malarias, Plasmodium knowlesi and P. falciparum. Sera from five Gambian adults who were highly immune to P. falciparum were used as a reagent to study the cross-reactivity between P. falciparum schizonts and surface proteins on P. knowlesi merozoites. Although the sera bound to the surface of viable, intact P. knowlesi merozoites, the sera did not block invasion of rhesus erythrocytes. 125I-lactoperoxidase-labeled surface proteins on merozoites formed complexes with the antibody. All major protein bands seen in the electrophoresis of the original Triton extract were bound by the immune sera. Because Gambians have never been exposed to P. knowlesi malaria, the antibodies that reacted with P. knowlesi merozoites must be directed against antigens of another parasite such as P. falciparum. We tested this hypothesis by competition for antibody in a Gambian serum between Triton-extracted antigens from P. falciparum schizont-infected erythrocytes and from surface-labeled P. knowlesi merozoites. P. falciparum inhibited the reaction, thus indicating cross-reaction between antigens in P. falciparum schizonts and P. knowlesi merozoites.
Human T lymphocyte subpopulations defined by Fc receptors and monoclonal antibodies. A comparison.
Authors: Reinherz E L , Moretta L , Roper M , Breard J M , Mingari M C , Cooper M D , Schlossman S F
Published: June 2004

Human T cell subpopulations have been defined on the basis of differential expression of either Fc receptors or specific cell-surface antigens. In this study, we utilized a series of monoclonal antibodies reactive with T cells, monocytes, and Ia antigens to characterize isolated subpopulations of T cells bearing receptors for the Fc portion of IgG (T gamma) and subpopulations of T cells bearing receptors for the Fc portion of IgM T mu. The results showed that the T mu population contained both inducer (OKT4+) and cytotoxic/suppressor (OKT5+) populations and was similar to the unfractionated T cell population, whereas the T gamma subset contained few T lymphocytes (OKT3+) and was not enriched for either T cell subset defined by these monoclonal antibodies. Rather, the T gamma population was comprised largely of Ia- cells possessing a monocyte antigen (OKM1+). In reciprocal studies, it was found that both isolated OKT4+ and OKT5+ T cell subsets contained few T gamma cells, whereas both subsets were mainly comprised of T mu cells. We conclude that there is little correlation between T cell subsets defined by these monoclonal antibodies and those defined by Fc receptors.
Regulation of the anti-inulin antibody response by a nonallotype-linked gene.
Authors: Stein K E , Bona C , Lieberman R , Chien C C , Paul W E
Published: June 2004

The antibody response to the inulin [(In), beta-(2 leads to 1) fructosan] determinant of bacterial levan [(BL), a beta-(2 leads to 6) polyfructosan that contains beta-(2 leads to 1) branch points] requires the presence of the a haplotype of the Igh gene complex. BALB/c (Igh a) mice immunized with BL produce IgG anti-In antibodies of a single spectrotype by isoelectric focusing analysis. C57BL/6 mice, which possess the b haplotype of the Igh gene complex and which fail to produce anti-In antibodies, nevertheless possess a gene, spectrotype regulation gene 1 (Sr-1), that regulates the isoelectric focusing (IEF) pattern of anti-In antibodies in mice of the a haplotype. Thus, the IEF patterns of anti-In antibodies of (BALB/c x C57BL/6)F1 mice and of B.C8 mice (C57BL/Ka . Igh-Ca) are considerably more complex than those of BALB/c. Backcross analysis indicates that Sr-1 is not linked to the Igh complex, the major histocompatibility complex, or to the genes that code for coat color. Studies of the heterogeneity of anti-In antibodies in recombinant inbred lines and their progeny from matings to BALB/c and C.B20 (BALB/c . Igh-Cb) suggest the existence of other regulatory genes.
Monoclonal rat anti-major histocompatibility complex antibodies display specificity for rat, mouse, and human target cells.
Authors: Smilek D E , Boyd H C , Wilson D B , Zmijewski C M , Fitch F W , McKearn T J
Published: June 2004

24 monoclonal rat antibodies are described that are reactive with determinants encoded by the major histocompatibility complex (MHC) of the rat. These hybridoma antibodies were derived by fusing mutant mouse myeloma cells to spleen cells from Lewis rats immunized with allogeneic Brown Norway cells. All 24 antibodies are cytotoxic for both Brown Norway target cells and target cells from the appropriate MHC congenic rats. Pattern of cytotoxicity and hemagglutination strongly suggest reactivity against class I (K or D equivalent) rat MHC determinants. Cytotoxic cross-reactivity patterns were generated for each monoclonal antibody on a panel of rat and mouse lymphoid cells and human peripheral T lymphocytes. A high degree of interspecies cross-reactivity was noted with approximately one-half of the antibodies positive on human and/or mouse target cells. 11 antibodies recognized polymorphic determinants in the mouse, and, by using target cells from MHC congenic mouse strains, it was shown that these determinants are encoded by genes within the H-2 complex. Finally, by considering the overall reactivity patterns of these monclonal antibodies on all target cells, one can show that these 24 antibodies represent a minimum of 14 antibody specificities.
Antigen receptors on major histocompatibility complex-restricted T lymphocytes. I. Preparation and characterization of syngeneic antisera against trinitrophenyl-activated T cell blasts and demonstration of their specificity for idiotypes on cytotoxic T lymphocytes.
Authors: Krammer P H , Rehberger R , Eichmann K
Published: June 2004

This paper describes the specificity of AKR anti-(a) [AKR anti-trinitrophenylated AKR (AKR-TNP)] [AKRa (AKRaAKR TNP)] antisera raised in syngeneic AKR mice against AKRaAKR-TNP cell populations enriched for H-2-restricted aTNP cytotoxic lymphocytes (CTL) by blast-cell isolation. The activity of the antisera resided in the Ig fraction. All antisera were shown to reproducibly react with AKRaAKR-TNP-CTL-containing cell populations in indirect immunofluorescence and all removed the major fraction of CTL in complement-dependent lysis causing a considerable depression of cell-mediated lympholysis. The antisera were nonreactive with alloreactive AKRaC57BL/6 CTL and other H-2-restricted AKR CTL against fluorescein-isothiocyanate-conjugated AKR-target cells. It could be excluded that the antisera contained contaminating antibodies against TNP, TNP-neoantigenic determinants (NAD), or processed CTL-receptor-bound TNP-NAD, thus demonstrating specificity for determinants on T cell receptors of AKRaAKR-TNP CTL. These receptors were produced by the CTL themselves. These observations are interpreted to suggest that AKRa (AKRaAKR-TNP) antisera contain anti-idiotypic antibodies directed against specificity-associated determinants (idiotypes) on T cell receptors of H-2-restricted AKRaAKR-TNP CTL. The antisera provide a new tool to study the genetic control of idiotype expression on H-2-restricted CTL, the biochemistry of T cell receptors, and the regulation of the generation of H-2 restricted CTL on the idiotype level.
Regulation of granulomatous inflammation in murine schistosomiasis. In vitro characterization of T lymphocyte subsets involved in the production and suppression of migration inhibition factor.
Authors: Chensue S W , Boros D L , David C S
Published: June 2004

Host granulomatous inflammation in murine schistosomiasis mansoni is a T cell-mediated immune response, which, at the chronic stage of the disease, undergoes T suppressor lymphocyte-dependent modulation. In the present study this phenomenon was further analyzed in vitro. Spleen cells of mice undergoing modulation (20 wk of infection) when mixed with spleen cells of animals exhibiting vigorous granulomatous responses (8 wk of infection) abrogated in vitro migration inhibition factor (MIF) production by the latter. Characterization of the delayed-type hypersensitivity T lymphocytes involved in lymphokine production showed that they belonged to the Lyt-1+ subset and did not express I region-encoded antigens. In contrast, T lymphocytes involved in the suppression of MIF activity belonged to the Lyt-2+ subpopulation of cells, which expressed I-J- and I-C-subregion determinants. These results suggest that the modulation of the granulomatous hypersensitivity response in mice is the result of T-T cell interaction with subsequent regulation of inflammatory lymphokine production.
The murine H-2.7 specificity is an antigenic determinant of C4d, a fragment of the fourth component of the complement system.
Authors: Ferreira A , David C S , Nussenzweig V
Published: June 2004

The S region of H-2 controls a polymorphism of the gamma-chain of C4 (gamma 1, gamma 2, and gamma 3) as shown by differences in their isoelectric points. The G region of H-2 was defined by the presence of an alloantigen (H-2.7) on erythrocytes and serum. We found that antisera to H-2.7 immunoprecipitated C4 and no other protein from mouse EDTA-plasma. Furthermore, all H-2.7-positive strains bear C4-gamma 1, and conversely, H-2.7-negative mice bear C4-gamma 2 or gamma 3 (with one exception; see below). The H-2.7 specificity resides on C4d, a 45,000-mol wt fragment generated from the cleavage of the alpha'-chain of C4b by serum control proteins. Because the C4d fragment bears the labile binding site of C4 for cell membranes, it is likely that the erythrocyte alloantigen is acquired from serum as a result of the activation of C4. On the basis of these findings, the existence of a separate G locus is unlikely. Our results also show that C4-gamma 1 and C4-gamma 2 differ from each other at least in their alpha- and gamma-chains, and may represent complex allotypes. No trans effects were observed in F1 hybrids between H-2.7-positive and -negative mice. Mice that bear the k allele in the S region are exceptional in two respects: they are C4-deficient and their C4 molecules bear gamma 2 chains and the H-2.7 alloantigen. Perhaps the low levels of C4 are a consequence of the genetic event leading to this unusual alpha-gamma-chain combination.
Different divalent cation requirements for binding IgM complexes to lymphocytes and macrophages.
Authors: Walia A S , Shaw D R , Fuson E W , Andersson B , Lamon E W
Published: June 2004

We have found that Mg++ supports IgM complex binding to mouse lymphocytes but not to macrophages. In contrast, Ca++ supports IgM complex binding to macrophages but not lymphocytes. IgG complex binding to both lymphocytes and macrophages is divalent cation independent. These findings allow one to distinguish IgG from IgM binding and macrophage from lymphocyte IgM complex binding by their differential divalent cation requirements.
Role of oxygen-dependent mechanisms in antibody-induced lysis of tumor cells by activated macrophages
Authors: Nathan C , Cohn Z
Published: June 2004

The alloantiserum-dependent lysis of TLX9 lymphoma cells by peritoneal cells from Bacille Calmette-Guerin (BCG)-treated mice was inhibited 62 percent by depletion of oxygen. This effect did not appear to be a result of interference with mitochondrial respiration because cyanide, azide, and dinitrophenol did not inhibit cytotoxicity. Preincubating the effector cells for 2 h without glucose, which markedly reduces their ability to release hydrogen peroxide, likewise suppressed antibody-dependent cytolysis by 62 percent. Lysis of sensitized lymphoma cells was virtually abolished by 6 mg/ml of thioglycollate broth, a concentration that also abrogated the detectable release of hydrogen peroxide and the lysis of lymphoma cells by BCG-activated macrophages in response to phorbol myristate acetate (PMA). This concentration of thioglycollate broth was not toxic to the effector cells, as judged by adherence to plastic, binding of opsonized erythrocytes, and phagocytosis of radiolabeled starch granules. Catalase, superoxide dismutase, horseradish peroxidase, mannitol, ethanol, benzoate, and diazabicyclooctane were without consistent effects. Cytochalasin B and dihydrocytochalasin B both markedly suppressed cytolysis, whether induced by antibody or by PMA (ID(50), 0.5 μg/ml). Cytoehalasin B was an equally potent suppressor of glucose uptake and PMA-induced hydrogen peroxide release by BCG-activated macrophages (ID(50), 0.5 μg/ml). However, dihydrocytochalasin B lacked these latter effects, which suggests that cytotoxicity required intact contractile elements. The extracellular lysis of antibody-coated lymphoma cells by BCG-activated macrophages appears to have a predominantly oxidative basis.
Identification of the membrane glycoprotein that is the C3b receptor of the human erythrocyte, polymorphonuclear leukocyte, B lymphocyte, and monocyte
Authors: Fearon DT
Published: June 2004

A human erythrocyte membrane glycoprotein of 205,000 mol wt (gp205) has been identified as the C3b receptor of the erythrocyte, polymorphonuclear leukocyte (PMN), B lymphocyte, and monocyte. Initially, gp205 was sought and characterized as a constituent of the human erythrocyte membrane that can impair activation of the alternative complement pathway by inducing loss of function of the properdin-stabilized amplification C3 convertase (C3b,Bb,P) through displacement of Bb from C3b and by promoting cleavage-inactivation of C3b by C3b inactivator. These inhibitory activities of gp205 suggested that this membrane glyeoprotein had an affinity for C3b and prompted an analysis of its possible identity as the C3b receptor of human peripheral blood cells. The F(ab')2 fragment of rabbit IgG anti-gp205 inhibited the formation of rosettes with sheep EC3b of human erythroeytes, B lymphocytes, monocytes and PMN in a dose-response manner; the 50 percent inhibitory doses were 0.13/μg/ml, 0.90 μg/ml, 1.25 μg/ml, and 1.20 μg/ml of F(ab')2, respectively. Anti-gp205 did not impair the formation of rosettes by monocytes and B lymphocytes with sheep EC3bi or with EC3d. Scatchard analysis of the number of specific (125)I-F(ab')(2) anti-gp205 binding sites/cell revealed 950 sites/erythrocyte, 21,000 sites/cell of B lymphocyte preparation, 57,000 sites/PMN, and 48,000 sites/monocyte, indicating that the higher concentrations of antibody that had been required for inhibition of rosette formation by the nucleated cells reflected larger numbers of receptors on these cells. Direct evidence for the identity of gp205 as the C3b receptor of the four cell types was obtained when detergent-solubilized membrane proteins of the surface-radioiodinated cells were reacted with anti- gp205 and the immunoprecipitate was analyzed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. In each instance, the antigenic material reacting with anti-gp205 represented a single protein with an apparent 205,000 mol wt. Thus, gp205 is the C3b receptor of human erythrocytes, PMN, B lymphocytes, and monocytes.
Suppression of antibody and T cell proliferative responses to L-glutamic acid60-L-alanine30-L-tyrosine10 by a specific monoclonal T cell factor.
Authors: Kapp J A , Araneo B A , Clevinger B L
Published: June 2004

The synthetic terpolymer L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) stimulates GAT-specific suppressor T cells in nonresponder mice. Extracts from these T cells contain a GAT-specific soluble T cell suppressor factor (GAT-TsF) that inhibits development of GAT-specific plaque-forming cell (PFC) responses by spleen cells from nonresponder mice stimulated with GAT complexed to methylated bovine serum albumin (GAT-MBSA). These extracts also contain a factor that inhibits development of GAT-specific proliferative responses by GAT-MBSA-primed, nonresponder lymph node T cells. Experiments reported in this manuscript show that a hybrid T cell line, produced by fusion of the AKR thymoma, BW5147, with spleen cells that contain GAT-specific suppressor T cells, produces a constitutive GAT-specific suppresor factor that functionally and serologically resembles GAT-TsF extracted from T cells. More importantly, both GAT-specific PFC and T cell proliferative responses are inhibited by this factor.