bluuebunny/crossref_metadata_2025_split huggingface dataset:
IL-3-dependent growth of basophil-like cells and mastlike cells from human bone marrow.
Authors: Kirshenbaum A S , Goff J P , Dreskin S C , Irani A M , Schwartz L B , Metcalfe D D 
Published: December 2022

Abstract
Human bone marrow cultured in the presence of human rIL-3 has been reported to give rise to basophils. In contrast, mouse bone marrow, cultured in the presence of mouse IL-3, leads to the growth of mast cells. To determine if human rIL-3 might also stimulate the growth of human mast cells, we cultured human bone marrow in the presence of human rIL-3 in suspension cultures, methylcellulose, and in "interphase" cultures where cells are layered over agar. The presence of mast cells was determined using a variety of histochemical techniques. In agreement with previous reports, basophil-like cells were identified in all culture systems. Mastlike cells were identified only in interphase cultures. By 3 wk, such cultures consisted of basophil-like cells (20 to 50%) and mastlike cells (1 to 5%). Cultures supplemented with rIL-4 showed no additional increase in basophil-like and mastlike cells. Both basophil-like and mastlike cells fluoresced with o-phthaldialdehyde and exhibited IgE receptors. Unlike basophil-like cells, mastlike cells were chloroacetate esterase, amidase, and human mast cell tryptase positive. We conclude that human rIL-3 can support the growth of human mastlike cells under selected culture conditions.
Differential effects of liposome-incorporation on liver macrophage activating potencies of rough lipopolysaccharide, lipid A, and muramyl dipeptide. Differences in susceptibility to lysosomal enzymes.
Authors: Daemen T , Veninga A , Dijkstra J , Scherphof G 
Published: December 2022

Abstract
We investigated the in vitro activation of rat liver macrophages to a tumor-cytotoxic state with muramyl dipeptide (MDP), rough LPS (Re-LPS) and lipid A in both a free and liposome-encapsulated form. The tumor cytotoxic state of the liver macrophages was determined with a [methyl-3H]thymidine release assay using C26 colon adenocarcinoma cells as target cells. As was shown previously, the encapsulation of MDP within multi-lamellar phospholipid vesicles greatly enhanced the activating potency of the drug; by contrast, encapsulation of Re-LPS or lipid A significantly reduced the activation of macrophages as compared to the free form of these agents. At a dose of 1 ng of free Re-LPS per ml a significant induction of tumor cell lysis was observed whereas a maximal level was obtained at a concentration of approximately 10 ng/ml. By encapsulation of Re-LPS in liposomes the activating potency diminished 20- to 100-fold. The minimal concentration required to induce detectable macrophage activation with free lipid A was 10 ng/ml, while liposome-encapsulated lipid A did not induce any detectable tumor cell lysis up to a concentration of 200 ng/ml. After a 1-h pre-incubation with a lysosomal fraction from rat liver at pH 4.8, the macrophage-activating potency of Re-LPS and lipid A was diminished by up to 95% whereas MDP remained fully active under these conditions. We conclude that, due to endocytic uptake of liposome-incorporated Re-LPS and lipid A and subsequent intralysosomal degradation, these immunomodulators are inactivated with respect to their potency to activate liver macrophages to tumor cytotoxicity.
Immune responses during human schistosomiasis mansoni. XVI. Idiotypic differences in antibody preparations from patients with different clinical forms of infection.
Authors: Montesano M A , Lima M S , Correa-Oliveira R , Gazzinelli G , Colley D G 
Published: December 2022

Abstract
Antibodies were purified from pooled sera from patients with different clinical forms of schistosomiasis mansoni on immunoaffinity columns of schistosome soluble egg Ag (SEA). As previously reported, T lymphocytes in PBMC preparations from schistosomiasis patients (but not control subjects who have never been infected) proliferate when cultured in the presence of certain of these anti-SEA purified antibodies. We now show that PBMC from most patients with chronic schistosomiasis, regardless of the clinical form of their infection, respond to anti-SEA antibodies from sera of asymptomatic (intestinal) or hepatointestinal patients. In stark contrast, none responds to anti-SEA antibodies purified from sera of acute or hepatosplenic patients. All of these multiclonal anti-SEA antibody preparations were active in anti-SEA ELISA assays and gave comparable patterns of reactivity with SEA upon immunoblotting analysis. Immunization of rabbits with some of these anti-SEA antibody preparations, followed by absorption of the rabbit antisera on absorbents of normal Ig, produced specific anti-Id reagents. Use of these reagents in competitive ELISA systems demonstrated that the Id in stimulatory and nonstimulatory anti-SEA antibody preparations differ with regard to the proportion of the serologically defined Id expressed by each. It appears possible to screen patients' plasmas for the presence of shared Id by use of suitable Id/anti-Id competitive ELISA assays. Taken together these data indicate that only certain Id-positive preparations are stimulatory to patients' PBMC, and the expression of these T cell stimulatory, immunoregulatory Id on anti-SEA antibodies correlates with the clinical form of a patient's infection.
Expression of macrophage p120 depends on early protein synthesis.
Authors: Johnston P A , Koerner T J , Jansen M M , Hamilton T A 
Published: December 2022

Abstract
We have previously identified a group of early proteins preceding the expression of a 120-kDa protein (p120) which coincides with tumoricidal activation in peritoneal macrophages. In the present report, we have asked whether the in vitro induction of new or enhanced expression of p120 depends on early protein synthesis and RNA synthesis during the treatment period. Expression of p120 was sensitive to pretreatment of the macrophages with either actinomycin D or cycloheximide, indicating that both active protein synthesis and RNA synthesis were required. When poly-adenylated RNA isolated from various macrophage populations was translated in a rabbit reticulocyte in vitro translation system, only mRNA isolated from cells which express p120 was able to direct synthesis of a 120-kDa polypeptide. This product showed identical mobility to p120 induced in intact activated macrophages radiolabeled with [35S]methionine. The presence of translatable p120 mRNA was dependent upon treatment of thioglycollate-elicited macrophages with both IFN-gamma plus LPS at low doses, as is expression of p120 in intact cells. Accumulation of translatable p120 mRNA was blocked by treatment with cycloheximide, indicating that active protein synthesis was required during the induction period. These results suggest that the presence of specific translatable mRNA encoding the p120 polypeptide is dependent upon the expression of early macrophage gene products.
Characterization of a monoclonal antibody which detects all murine alpha beta T cell receptors.
Authors: Kubo R T , Born W , Kappler J W , Marrack P , Pigeon M 
Published: December 2022

Abstract
Research on the specificities, functions, and maturation of T cells would be greatly aided by a collection of monoclonal antibodies which distinguishes different types of TCR. With this end in mind hamsters were immunized and tested for production of pan-reactive anti-mouse alpha beta TCR antibodies. In this report we describe the properties and uses of a mAb, H57-597, produced from one of these animals. The mAb reacts with surface receptors on all alpha beta TCR-bearing cells and does not react with receptors on gamma delta+ T cells. In an immobilized form, this antibody can directly activate T cells bearing alpha beta TCR. It can be used in immunoprecipitation reactions to precipitate receptor from the appropriate cell types. In combination with anti-CD3, the antibody can be used in cytofluorographic analyses to measure numbers of CD3+, alpha beta+, and CD3+, gamma delta+ cells in the thymus and periphery.
Human IgM molecules that bind staphylococcal protein A contain VHIII H chains.
Authors: Sasso E H , Silverman G J , Mannik M 
Published: December 2022

Abstract
Staphylococcal protein A (SPA) is a bacterial membrane protein which has distinct binding sites for Fc gamma and for the Fab region of some IgM, IgG, IgA, and IgE molecules. This study establishes a structure-function correlation responsible for the binding of Ig Fab regions to SPA. Binding of 24 isolated human monoclonal IgM proteins to SPA was measured in a solid phase RIA. VH and V kappa subgroups of each IgM were determined by SDS-PAGE, transfer blotting, and detection with antisera prepared against specific first framework region peptides. Binding to SPA was seen with 10 of 11 VHIII IgM, but none of the 7 VHI or 6 VHII. Similarly, polyclonal IgM fractionated on a SPA-Sepharose CL4B column showed nearly complete partition of VHIII molecules into the SPA-binding fraction, and VHI and VHII subgroup proteins into the fall-through. We conclude that SPA binding is a functional marker for VHIII H chains in human IgM molecules.
Induction of murine hemopoietic growth factors by toxic shock syndrome toxin-1.
Authors: Galelli A , Anderson S , Charlot B , Alouf J E 
Published: December 2022

Abstract
Toxic shock syndrome toxin-1 (TSST-1), an extra-cellular 22 kDa single chain protein produced by most Staphylococcus aureus strains isolated from patients with toxic shock syndrome (TSS), induces modifications of blood cell values similar to those observed during TSS. We therefore analyzed the effects of TSST-1 on the proliferation and differentiation of murine granulocyte-macrophage progenitor cells (CFU-culture) and the eventual role of endotoxin in this response. TSST-1 had no direct effect on the proliferation of CFU-culture and was unable to influence the CSF-induced proliferation and differentiation of these progenitors. In contrast, TSST-1 was a potent inducer in spleen cell cultures of a factor with an ability to induce both colony formation by bone marrow cells and proliferation of an IL-3-dependent cell line. Nanogram amounts of TSST-1 were able to induce the release of CSF activity in spleen cell cultures from both normal and LPS-hyporesponsive mice. Cells from C3H/HeJ mice were as responsive as cells from C3H/He Pas mice. Furthermore, in spleen cell cultures from normal mice, TSST-1 and LPS did not act synergistically to induce CSF activity. Nanogram amounts of TSST-1 were also able to induce CSF activity in vivo but failed to induce IL-3 activity in the serum and organ-conditioned media from TSST-1-treated mice.
Isolation and characterization of the highly immunogenic cell wall-associated protein of Mycobacterium leprae.
Authors: Hunter S W , McNeil M , Modlin R L , Mehra V , Bloom B R , Brennan P J 
Published: December 2022

Abstract
In a recent study, we demonstrated that certain reactivities crucial to the immune response in leprosy are due to protein associated with the cell wall peptidoglycan "core" of Mycobacterium leprae. We now describe a primary method for the isolation of a highly immunogenic, large molecular-size, cell wall protein (CW-P) complex from M. leprae, freed of soluble proteins, bound mycolates, arabinogalactan, and much of the peptidoglycan. The complex is of apparent relative molecular size 2 x 10(6) to 20 x 10(6) Da, is distinguished by a high content of Ala, Gly, Leu, Asx, and Glx, and some peptidoglycan, and represents up to 7% of the bacterial mass. It is stable to a variety of dissociation and reductive processes and, in accord with its size, is not resolvable by polyacrylamide gel electrophoresis. The mAb to the CW-P complex also react with the heat shock 65-kDa protein of M. leprae. Conversely, antibodies that recognize internal epitopes within the polypeptide chain of the heat shock protein also react with CW-P; however, antibodies that recognize the N and C termini of the 65-kDa protein fail to react with CW-P, and some anti-CW-P mAb do not recognize any of the soluble proteins of M. leprae. Alternate methods to derive the large peptidoglycan-associated protein result in lower yield and less of the associated heat shock protein, implying that the 65-kDa protein may not be crucial to the immunogenicity of the complex. In an accompanying paper, we demonstrate that T cell clones raised to CW-P also selectively recognize soluble proteins, primarily of 7-kDa and 16-kDa size. Thus, the image of the CW-P complex of M. leprae is of a few immunoreactive polypeptides in avid association with a modicum of peptidoglycan to which the 65-kDa polypeptide may be variably attached, perhaps due to involvement in assembly of the complex.
Molecular analysis of H-2-deficient lymphoma lines. Distinct defects in biosynthesis and association of MHC class I heavy chains and beta 2-microglobulin observed in cells with increased sensitivity to NK cell lysis.
Authors: Ljunggren H G , Pääbo S , Cochet M , Kling G , Kourilsky P , Kärre K 
Published: December 2022

Abstract
It has previously been reported that MHC class I-deficient RBL-5 and YAC-1 lymphoma sublines show an enhanced NK sensitivity in vitro. In the present study such lymphoma variants were found to have different defects in H-2 biosynthesis such as 1) reduced beta 2-microglobulin and H-2 H chain transcription, 2) block in beta 2-microglobulin translation, and 3) impaired association between beta 2-microglobulin and H-2 H chains. For lines with the latter two defects, the results suggested that a major part of the H chains were arrested before the middle Golgi complex as indicated by their failure to undergo carbohydrate side chain trimming. The data suggest that NK sensitivity can be directly influenced by the membrane expression of MHC class I gene products of tumor targets because three independent molecular defects, all interfering with the cell surface H-2 expression, gave rise to NK-sensitive phenotypes. These variant lines will also be useful tools for studies of H-2 glycoprotein assembly and transport and for Ag presentation to CTL.
Molecular defects in the non-expressed H-2 E alpha genes of the f and q haplotypes.
Authors: Vu T H , Begovich A B , Tacchini-Cottier F M , Jones P P 
Published: December 2022

Abstract
The expression and sequences of the mouse MHC class II genes, E alpha f and E alpha q, have been studied to determine the molecular basis for their defective expression. Previous work in our laboratory showed that H-2f and H-2q mice produce no detectable E alpha protein. Northern blot analysis confirms previous results showing normal amounts of E alpha f message and a 100-fold reduction in E alpha q mRNA. Despite that observation, the rates of transcription of both defective E alpha genes, measured by nuclear run-on transcription assays, are comparable to that of the normally expressed E alpha k gene. The nucleotide sequences of the E alpha f and E alpha q genes reveal mutations generating premature translation stop codons in both genes. A single base substitution has created the stop codon TGA at amino acid -2 in the E alpha f leader sequence. A nucleotide insertion at codon 64 in the second exon of the E alpha q gene results in a frame shift and a premature stop codon at amino acid residue 69 of a mature E alpha protein. The low steady state level of E alpha q mRNA may be correlated with the unusual size distribution of the RNA, possibly due to altered RNA processing.
Alpha beta T cell receptor and CD3 transduce different signals in immature T cells. Implications for selection and tolerance.
Authors: Finkel T H , Marrack P , Kappler J W , Kubo R T , Cambier J C 
Published: December 2022

Abstract
Ligand binding to alpha beta TCR has different consequences in thymocytes at different developmental stages, causing alternatively positive selection, clonal deletion, or activation. These various functional consequences may be due to changes in the signaling properties of the receptor complex during development. In this report we show that alpha beta TCR engagement on immature thymocytes has different effects on intracellular free calcium concentrations than alpha beta TCR engagement on mature T cells. In contrast, CD3 engagement on immature thymocytes and mature T cells has the same effect on intracellular free calcium, suggesting that altered signal transduction in immature thymocytes may be due to inefficient alpha beta TCR-CD3 coupling. These studies also suggest that in certain T cell populations, activation events resulting from ligation of CD3 may not accurately reflect the activation events resulting from ligation of the physiologic receptor, alpha beta TCR.
A 19-kDa human erythrocyte molecule H19 is involved in rosettes, present on nucleated cells, and required for T cell activation. Comparison of the roles of H19 and LFA-3 molecules in T cell activation.
Authors: Groux H , Huet S , Aubrit F , Tran H C , Boumsell L , Bernard A 
Published: December 2022

Abstract
We have previously described a molecule on the SRBC surface which, in addition to the sheep equivalent of LFA-3, is involved in the process of rosette formation. It is made of a single, 14- to 19-kDa, polypeptide chain, and we termed this molecule S14. We have now identified, on the human E a molecule with a similar Mr albeit somewhat higher (19 kDa). The mAb against H19 efficiently block autologous or homologous rosettes by binding to human E. In addition, purified H19 molecules block rosettes made with human E and SRBC in a dose-dependent manner. The H19 molecule, like LFA-3, is not limited to the E surface, but is also present on many nucleated cells, including T cells and monocytes. Moreover H19, like LFA-3, is required for T cell activation: when we stimulated whole PBMC anti-H19 blocked [H3]TdR incorporation triggered via CD3, but not via CD2, in contrast to anti-LFA-3 that inhibited activation via both pathways. When a mixture of highly purified T-PBL and autologous paraformaldehyde fixed accessory cells (AC) was cultivated, anti-H19 or anti-LFA-3 mAb bound to AC blocked T cell proliferation. When high amounts of rIL-1 (100 U/ml) were added to purified T-PBL, no AC were required to sustain their proliferation upon stimulation via CD2, contrary to stimulation via CD3. When lower amounts of rIL-1 (10 U/ml) were used, fixed AC were still necessary to sustain proliferation via CD2. In this latter situation, anti-H19 mAb bound to AC could no longer inhibit T cell proliferation, whereas the anti-LFA-3 mAb was still inhibitory. When T-PBL were stimulated via CD2 in the presence of 100 U/ml of rIL-1, anti-LFA-3 did not induce any inhibition. Thus the inhibitory effect of anti-H19 and anti-LFA-3 mAb can both be accounted for by an effect on the AC molecules only, and not on the T cell molecules. F(ab')2 fragments of anti-H19 mAb produced the same pattern of inhibition as the whole Ig molecule, excluding an effect via the FcR. Moreover, purified preparations of the H19 molecules also produced inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)
Anti-DNA antibodies bind directly to renal antigens and induce kidney dysfunction in the isolated perfused rat kidney.
Authors: Raz E , Brezis M , Rosenmann E , Eilat D 
Published: December 2022

Abstract
The pathogenesis of SLE is commonly attributed to the deposition of circulating immune complexes consisting of DNA and anti-DNA autoantibodies. However, recent work has shown multiple cross-reactions between anti-DNA antibodies and a variety of cellular and extracellular Ag. To test the possibility that these antibodies interact directly with glomerular Ag and induce kidney dysfunction, we applied mouse and human anti-DNA IgG to the isolated perfused rat kidney. The NZB/NZW mouse monoclonal anti-DNA bound to glomerular Ag with a concomitant induction of proteinuria and a decrease in inulin clearance. The albumin excretion was 2301 +/- 734 micrograms/min at 160 min of perfusion, as compared with 85 +/- 21 micrograms/min in controls (p less than 0.001). The inulin clearance was reduced to 0.17 +/- 0.02 ml/min as compared with 0.28 +/- 0.09 ml/min in controls (p less than 0.05). Polyclonal anti-DNA IgG obtained from patients with lupus nephritis bound to rat glomeruli and induced albumin excretion of 542 +/- 217 micrograms/min at 160 min of perfusion, as compared with 163 +/- 77 micrograms/min in controls (p = NS). The addition of plasma as a source of C to the human IgG increased the proteinuria markedly (albumin excretion of 1115 +/- 195 micrograms/min at 160 min of perfusion, p less than 0.02), probably due to C activation. Preincubation of the reactive mouse and human IgG with DNA completely abolished their binding to renal tissue and its physiologic consequences. These results suggest that direct binding of anti-DNA antibodies to renal Ag may play an important role in the induction of lupus nephritis.
Activation by IL-2, but not IL-4, up-regulates the expression of the p55 subunit of the IL-2 receptor on IL-2- and IL-4-dependent T cell lines.
Authors: Jankovic D L , Gibert M , Baran D , Ohara J , Paul W E , Theze J 
Published: December 2022

Abstract
We have investigated the effects of IL-2 and IL-4 on different parameters of T cell activation using three T cell lines. The Th cell line L14 and the cytotoxic T cell line C30.1, both grown in IL-2-containing medium, and a line derived from C30.1 cells (line 1) cultured in IL-4 for a prolonged period were studied. All three cell lines could be activated with IL-2 or IL-4. T cell stimulation by either IL-2- or IL-4-induced identical patterns of cell size enlargement and transferrin receptor expression. However, only IL-2 up-regulated cell-surface expression of the p55 subunit of the IL-2R (p55 IL-2R) as measured by flow cytometry and RIA. This difference was also reflected by the accumulation of soluble p55 IL-2R in the culture medium. No significant increase in expression of membrane or soluble forms of p55 IL-2R was detected after IL-4 stimulation. mAb specific for p55 IL-2R which block IL-2-induced T cell growth did not affect IL-4-mediated T cell proliferation indicating that p55 IL-2R is not involved in IL-4-mediated T cell growth. Analysis of IL-4R expression performed on line 1 using biotinylated IL-4 revealed that IL-4, but not IL-2, is capable of increasing IL-4R expression. Together these results suggest that during IL-2- or IL-4-induced T cell proliferation, each lymphokine specifically up-regulates its own receptor.
Characterization of the baboon erythrocyte C3b-binding protein.
Authors: Birmingham D J , Cosio F G 
Published: December 2022

Abstract
E from primates demonstrate type 1 CR (CR1) with binding specificities for C3b and C4b. In the present study we characterized the E C3b-binding protein of baboons. We showed that three out of four mouse mAb and one polyclonal antiserum, raised against human E CR1, cross-reacted with baboon E. In addition, one anti-human CR1 mAb (1B4) and a polyclonal anti-human CR1 inhibited the binding of C3b opsonized immune complexes to baboon E. Finally, a mAb to human CR1 (E11) recognized epitopes on E of a variety of nonhuman primates, including baboons. SDS-PAGE analysis of biochemically purified baboon E membrane fractions reactive with E11 demonstrated a 65-kDa protein as a major component. Affinity absorption and elution experiments verified this protein to be E11 reactive as well as a C3b binding protein. E surface radiolabeling, followed by C3i affinity purification, confirmed that this 65-kDa protein is the only C3b-binding protein present on the baboon E membrane. We postulate that the baboon E 65-kDa protein is the equivalent of the human E CR1. In addition, there appear to be antigenic similarities between the baboon E 65-kDa protein and the human E CR1.