bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metabolism of immunoglobulin A in lactating mice: origins of immunoglobulin A in milk
Authors: Halsey John F. , Mitchell Craig , Meyer Robyn , Cebra John J. 
Published: February 2007

AbstractThe metabolism of albumin and IgA was studied in normal and lactating mice. Lactation resulted in significant changes in the metabolism of these proteins. The serum albumin concentration was lowered from 47 mg/ml in normals to 24 mg/ml in lactating mice. However, only a slight decrease in the serum concentration of IgA was observed during lactation. The proportion of polymeric and monomeric IgA in serum and milk was evaluated by gel exclusion chromatography. The onset of lactation led to a rise in the proportion of polymeric IgA (P‐IgA) in serum from 37% to 51%. The proportion of P‐IgA in milk was 65% and remained constant throughout lactation. P‐IgA and albumin were shown to be efficiently transferred from the serum of lactating mice into their milk. Serum decay studies were performed to evaluate the turnover of the serum pools during lactation. The rates of disappearance from the serum of isotopically labeled albumin and P‐IgA were observed to increase dramatically during lactation, suggesting that both of these two milk proteins might be derived at least in part from the serum. The sites of synthesis of milk IgA (local vs. extra‐mammary gland) were evaluated by determining the extent of dilution of isotopically labeled serum IgA during transport through the mammary gland into the milk. Early in lactation, the majority of the IgA in mouse milk appeared to be derived from distant sites and transferred via the blood to the mammary gland. However, by day 8 of lactation, the isotopically labeled P‐IgA in milk was significantly.diluted by the IgA synthesized in the mammary gland. Albumin and IgG were not diluted by local synthesis indicating that these proteins were exclusively serum‐derived.
A systemic lupus erythematosus (SLE)‐like disease in mice induced by abnormal T‐B cell cooperation. Preferential formation of autoantibodies characteristic of SLE
Authors: Gleichmann Ernst , Van Elven Evert H. , Van Der Veen J. P. W. 
Published: February 2007

AbstractThis is the first report describing the experimental induction of a full‐blown clinical syndrome strongly resembling systemic lupus erythematosus (SLE). The method used was the induction of a chronic graft‐vs.‐host reaction (GVHR) employing genetically nonautoimmune strains of mice. Many of the F1 mice undergoing a GVHR (GVH F1 mice) revealed the following pathological alterations: splenomegaly, periarteritis, immunecomplex glomerulonephritis accompanied by elevated proteinuria and ascites, dysgammaglobulinemia, persistently increased production of IgG in the spleen, and formation of autoantibodies to thymocytes, erythrocytes, nuclear antigens, double‐stranded DNA, and antibodies deposited along the basement membrane of skin.In spite of the excessive T cell help, the GVH F1 animals failed to produce spontaneous serum antibodies to dextran and the bacteriophage fd. They also had no increased numbers of spontaneous indirect plaque‐forming cells to sheep red blood cells and trinitrophenyl. These negative findings indicate that antigen has to be present during the GVHR to trigger antibody formation. This in turn suggests that the persistent presence of self‐antigens was essential for the formation of IgG autoantibodies in GVH F1 mice. However, whereas autoantibodies typical of SLE were readily produced, none of the GVH F1 mice had autoantibodies to thyroglobulin, or other autoantibodies not typical of SLE.Conceivably, not only the presence of self‐antigens, but also their antigenic configuration, may determine whether or not autoreactive B cells are successfully triggered during abnormal T‐B cell cooperation. Given the lack of carrier‐specific T helper cells in abnormal T‐B cell cooperation, protein self‐antigens, such as thyroglobulin, may be intrinsically less apt than the self‐antigens involved in SLE to bind to the corresponding autoreactive B cells. The self‐antigens involved in SLE, such as DNA and cell‐surface epitopes, are assumed to be capable of multipoint high‐avidity binding to and cross‐linking of the Ig receptors of these B cells, thus providing an effective signal 1.
Polymorphism of a Qa‐1‐associated antigen defined by cytotoxic T cells. I. Qed‐1a and Qed‐1d
Authors: Lindahl Kirsten Fischer , Hausmann Barbara , Flaherty Lorraine 
Published: February 2007

AbstractTlad mice have a distinct Qed‐1 allele, Qed‐1d. Its product is detected by cytotoxic T cells raised in C57BW6 (H‐2b, Tlab) mice against cells from a new recombinant, B6‐TL.123+ (H‐2b, Tlad/b). Qed‐1d is also found on cells from B10.M, A.CA and B10.STC90 mice. It cross‐reacts weakly with Qed‐1b. (C57BL/6 X BALB/c) F1 anti‐B10. A (SR) effectors discriminate Qed‐1a and Qed‐1d, while C3H/HeJ anti‐B10. BR effectors cross‐react extensively. CB6F1 anti‐5R effector cells also discriminate between the Qed‐1 antigens of B6‐Tlaa (H‐2b, Tlaa) and those of B10. BR and other H‐2k, Tlaa strains.
Ontogeny of acquired immunological tolerance to H‐2 alloantigens
Authors: Wood Peter J. , Wayne Streilein J. 
Published: February 2007

AbstractThe ontogeny of mixed lymphocyte reaction and cell‐mediated lymphocytotoxicity (CML) responsiveness was studied in mice that had been neonatally tolerized by the injection of 15 × 106 semiallogeneic bone marrow and spleen cells, and compared to that of unprimed littermates. Spleen cells from primed mice did not develop reactivity towards the tolerizing antigen but did develop reactivity towards third‐party alloantigens. Similarily, thymus cells from primed mice also failed to develop CML reactivity towards the tolerizing antigen. Thymus cell mixed lymphocyte reactivity, which was demonstrable in neonates before the tolerizing injection, declined rapidly between 2 and 4 days of age, compared to that of controls. Thus neonatal tolerance was shown to operate at least at a thymic, and perhaps pre‐thymic level; measurement of the levels of chimeric cells in the thymus and bone marrow favored the latter interpretation.
Human natural killer‐like activity against mouse spleen cells
Authors: Yamamoto Janet K. , Edwin Blalock J. , Johnson Howard M. 
Published: February 2007

AbstractUnstimulated human peripheral lymphocytes were cytotoxic for normal mouse spleen cells and suppressed the in vitro antibody plaque‐forming cell (PFC) response of these cells to sheep red blood cells and dinitrophenylated Ficoll. The cells in the lymphocyte population that were responsible for the immunosuppression had properties of natural killer (NK) or NK‐like cells in that they were: (a) non‐E‐rosetting, (b) nonadherent, (c) unaffected by treatment with anti‐human immunoglobulin plus complement, (d) cytotoxic against an established human NK target, K562 leukemic cells, and (e) partially inactivated by mitomycin C. Addition of the human NK‐like cells to mouse spleen cell cultures at the time of antigen addition and at an effector cell to target cell ratio as low as 0.67:1 resulted in 85 to 96% suppression of the PFC response. Addition of NK‐like cells to cultures 18 h before harvesting in 5‐day cultures required higher concentrations and ratios (2.7 : 1) of effector to target cells to significantly suppress the PFC response. The data suggest that human NK‐like activity in suppression of the mouse PFC response is due to killing of the targets. The mouse spleen cell PFC system represents a potential model for assessment of human NK activity that is quite dramatic in its effect and can be used in addition to the well known 51Cr‐release assay. Also, since the mouse spleen cell is a normal cell, it provides a model in the PFC system for studying the mechanism of NK regulation of normal cellular function. An additional finding of this study was the observation that E‐rosetting T cells significanty enhanced the mouse PFC response. Thus, human peripheral lymphocytes contain discrete cellular populations that either enhance or suppress the mouse PFC response.
Mouse monoclonal antibodies against rat major histocompatibility antigens. Two Ia antigens and expression of Ia and class I antigens in rat thymus
Authors: Fukumoto Tetsuo , Robert McMaster W. , Williams Alan F. 
Published: February 2007

AbstractA rat Ia (RT‐1B) antigen (called Ia‐A) equivalent to the mouse I‐A product has been defined with mouse monoclonal antibodies (W. R. McMaster and A. F. Williams, Eur. J. Immunol. 1979. 9: 426). To identify other Ia antigens mouse monoclonal antibodies were raised against rat spleen glycoproteins depleted of the Ia‐A antigen. An IgG antibody (called MRC OX 17) was obtained and used to purify a molecule which had a similar structure to the Ia‐A antigen and reacted with anti‐Ia alloantibodies. There was no cross‐reaction between the two Ia glycoproteins in assays with mouse monoclonal antibodies, alloantibodies or rabbit antibodies. In one alloantiserum almost all the detectable anti‐Ia antibodies reacted with a mixture of the two Ia glycoproteins. The MRC OX 17 antibody did not bind to mouse cells, but rabbit antibodies to the pure rat glycoprotein cross‐reacted and recognized determinants mapping to the mouse I‐E region. In the thymus the rat Ia‐E antigen was on cortical epithelial and medullary reticular cells.An IgG monoclonal antibody (MRC OX 18) to isotypic determinants of rat histocompatibility RT‐1A antigens was also produced and used to analyze these antigens on thymus cells. The heavily labeled thymocytes were those with characteristics of mature T lymphocytes. Cortical epithelial cells and medullary dendritic‐like cells were also RT‐1A positive.
Expression of 20α‐hydroxysteroid dehydrogenase in nonlymphoid hemopoietic cell lines
Authors: Garland J. M. , Lanotte M. , Dexter T. M. 
Published: February 2007

AbstractExpression of 20α‐hydroxysteroid dehydrogenase (20α‐SDH), a putative T cell marker. has been examined in a number of nonlymphoid hemopoietic cell lines. Both promyelocytic and stromal bone marrow lines expressed significant 20α‐SDH activity which was not correlated with virus infection or growth rate. 20α‐SDH therefore is not a unique marker for T cells in hemopoietic tissues. This result is discussed in relationship to the action of the newly proposed interleukin 3.
Expression of HLA‐DR and common acute lymphoblastic leukemia antigens on glioma cells
Authors: Carrel Stefan , De Tribolet Nicolas , Gross Nicole 
Published: February 2007

AbstractThe expression on several established human glioma cell lines of two well‐defined differentiation antigens, HLA‐DR and the common acute lymphoblastic leukemia antigen (CALLA) has been demonstrated. Rabbit anti‐CALLA antiserum and monoclonal anti‐la antibodies specifically lysed glioma cells in the presence of complement. Absorption of anti‐CALLA antiserum and anti‐Ia antibodies by glioma cells abolished their cytotoxicity against blasts isolated from a common acute lymphoblastic leukemia. Immunoprecipitation of solubilized glioma cells by monoclonal anti‐Ia antibodies revealed two polypeptide chains of 28 and 33 kDa, whereas the anti‐CALLA antiserum precipitated a single polypeptide chain of 100 kDa.
Lymphocyte specificity to protein antigens V. Conformational dependence of activation of cytochrome c‐specific T cells
Authors: Buchmu Yolande , Corradin Giampietro 
Published: February 2007

AbstractVariations in the immunogenic and antigenic properties of native and denatured forms of cytochrome c were observed depending on the strain of mouse tested. In C57BL/6 and (C57BL/6 X DBA/2)F1 (BDF1 mice, priming with either native or denatured cytochrome c (apocytochrome c) gave rise to T cell blasts responding in a similar fashion to the two forms of the antigen and to different peptides derived from CNBr cleavage of the protein when tested for proliferation in the presence of C57BL/6 or BDF1 accessory cells. A different pattern of proliferation was observed when apocytochrome c‐specific DBA/2 or BDFl T cell blasts were tested with DBA/2 accessory cells. In this case, no response was obtained to heme peptide 1‐65. This was not due to an inability of DBA/2 macrophages to process and present heme peptide 1‐65, as they were able to present this antigen to native cytochrome c‐specific BDF1 T cell blasts. Thus, it seems that different sets of clones are generated upon priming BDF1 mice with denatured cytochrome c which are able to recognize different sets of peptides depending on the nature of the accessory cells. The results obtained are consistent with the hypothesis that degradation and presentation of native and denatured cytochrome c by macrophages is dependent on the three‐dimensional conformation of the protein.
Syngeneic sensitization of mouse lymphocytes on monolayers of thyroid epithelial Cells. II. T and B cell involvement in primary responses
Authors: Charreire Jeannine 
Published: February 2007

AbstractUsing a previously developed in vitro model of sensitization of lymphoid cells against monolayers of syngeneic thyroid epithelial cells, the T or B nature of the population involved in the primary response has been investigated. For this purpose normal good responder CBA strain mice were used. T cell participation was clearly demonstrated in two ways: first, by the loss of primary sensitization after T cell depletion accomplished using several different techniques (including in vivo and in vitro anti‐Thy‐1.2 treatment, hydrocortisone and cyclophosphamide injections) and second, by the high response (measured by tritiated thymidine uptake) of T cell‐enriched suspensions obtained either by nylon wool filtration or Ig‐anti‐Ig columns.
Lectin‐binding proteins as potent mitogens for B lymphocytes from nu/nu mice
Authors: Gebauer Günter , Schimpl Anneliese , Rüdiger Harold 
Published: February 2007

AbstractIt was found that lectin‐binding proteins (LB) from leguminosae seeds can serve as mitogens for B lymphocytes from athymic nu/nu mice. Most of the experiments were performed using a LB from Vicia faba as this was the most potent mitogen among all LB tested. When mixed B and T lymphocyte populations were stimulated by LB, a bell‐shaped dose‐response curve resulted which is also characteristic of the corresponding lectins; LB, however, act at much higher concentrations than the lectins. In control experiments, using lymphocytes from C3H/HeJ mice which have a genetic defect with respect to lipopolysaccharide responsiveness, the enhancement of DNA synthesis by LB was comparable to that observed with other strains. This indicates that stimulation by LB does not result from contamination by lipopolysaccharides. B lymphocytes from nu/nu mice were stimulated by LB as efficiently as mixed T and B lymphocyte populations whereas lectins per se had no effect on nu/nu lymphocytes.Cyclosporin A, a fungal metabolite, is known to specifically suppress T cell responses. Cyclosporin A did not influence the mitogenic activity of the LB from Vicia faba on unseparated spleen cells. Cell populations enriched for T cells (lymph node cells: nylon wool‐passed or nylon wool‐passed and anti‐Ia plus complement‐treated) responded poorly to LB, if at all, even in the presence of interleukin 2‐containing supernatants.
Production of IgG‐specific auto‐anti‐allotypes in b4.2‐suppressed rabbits
Authors: Naessens Jan , Vaeck Mark , De Smet Walter , Kulics Judit , Hamers Raymond 
Published: February 2007

AbstractRabbits were completely suppressed for kappa chain allotype b4.2, and autoantibodies against b4.1 or b4.2 could be raised in 2 out of 3 animals. The animal immunized with b4.1 produced anti‐b4 and anti‐Ms3, two activities which have never as yet been found together in one antiserum.Both autoantisera lacked the capacity to bind b4.2‐IgM, whereas they precipitated b4.2‐IgG very well. In one animal, anti‐b4 IgM activity appeared after the sixth immunization, at the age of 14 months. Allotype suppression was maintained in both rabbits till the end of their lives whereas all control animals recovered within 6 months. The autoantisera which were specific for b4 IgG could not induce suppression in vivo. However, specific inhibition of b4 IgG secretion was observed in vitro.
A human‐human hybridoma system based on a fast‐growing mutant of the ARH‐77 plasma cell leukemia‐derived line
Authors: Edwards Paul A. W. , Smith Clare M. , Neville A. Munro , O'hare Michael J. 
Published: February 2007

AbstractA rapidly‐growing, HAT‐sensitive cell line LICR‐LON‐HMy2 has been derived from the ARH‐77 human plasma cell leukemia‐derived line. It lacks the enzyme hypoxanthine phosphoribosyltransferase (EC 2.4.2.8). Hybrids have been reproducibly made for more than a year and in independent laboratories with lymphocytes from tonsils, lymph nodes and peripheral blood and tonsil lymphocytes cultured with antigens. The parent line and hybrids are very robust in culture and double in 20‐30 h. Hybrids clone easily and have stable karyotypes, most with modal numbers in the sixties. Stable Ig secretion patterns have been observed over 20‐30 passages, and after cloning. It was estimated that about half the hybrids produce new immunoglobulin chains in addition to the parent cell line's IgG1 (× light chain). High, but not limiting, density hybridoma cultures (approximately 5 × 105 cells/ml) typically produce 0.25‐2 μg/ml immunoglobulin per day, but some hybrids produce more. A high‐secreting variant of LICR‐LON‐HMy2 has been derived. The LICR‐LON‐HMy2 line is human and is distinct from the HAT‐sensitive human B cell‐lines SKO‐007 and GM 1500‐6TG A1 2. It is available for distribution.
Immune characteristics of graft rejection in nemerteans of the genus Lineus
Authors: Langlet Claude , Bierne Jacques 
Published: February 2007

AbstractThe rejection of xenogeneic grafts in marine worms of the genus Lineus (Nemertea) gives evidence for the occurence of immune mechanisms in these invertebrates. First, second‐set response is anamnestic with a three‐month memory component. Second, the accelerated rejection of second‐set grafts occurs anywhere in the body of the recipient, that is to say it is systemic. Third, the anamnestic response is species‐specific since it takes place only when second grafts are from donors of the same species as that of the first set. It is therefore plausible that the reaction to xenogeneic grafts is a cell‐mediated immune mechanism and that the self‐nonself discrimination may be a function of nemertean cells specialized for recognition at the species level and for memory.
Anti‐nuclear matrix antibodies in mixed connective tissue disease
Authors: Salden Martin H. L. , Van Eekelen Chris A. G. , Habets Winand J. A. , Vierwinden Gertie , van de Putte Leo B. A. , van Venrooy Walther J. 
Published: February 2007

AbstractPurified serum antibodies of patients suffering from mixed connective tissue disease were tested for their immunological specificity against nuclear constituents of HeLa S3 cells. In the indirect immunofluorescent staining technique, using cells and nuclei as targets, a typical speckled intranuclear staining pattern was obtained, that persisted after degradation and extraction of all nucleic acids and their associated proteins. This treatment of nuclei with detergents, DNase, RNase and high salt concentrations leave intact only the so‐called nuclear matrix which is an intranuclear proteinaceous network. Further proof that nuclear matrix proteins were targets of the autoimmune reaction was obtained after separation of these proteins by sodium dodecyl sulfate polyacrylamide gel electrophoresis and electrophoretic transfer to nitrocellulose (blotting). A specific number of blot‐transferred matrix proteins reacted with purified serum antibodies of 10 patients with mixed connective tissue disease, whereas this reaction was negative with normal healthy individuals. IgG preparations of 7 patients with systemic lupus erythematosus showed a weak, if any, reaction with matrix constituents. Obviously, in some connective tissue diseases serum antibodies are expressed which are directed to specific nuclear matrix antigens.
Construction of a partial rabbit spleen cDNA library and identification of immunoglobulin clones
Authors: Pavirani Andrea , Mage Rose , Jacobsen Frederick W. , Reddy E. Premkumar , Bernstein Kenneth , Fitzmaurice Leona 
Published: February 2007

AbstractA partial cDNA library was constructed from total poly A(+)‐RNA isolated from the spleen of a rabbit (kappa allotype b5; heavy chain allotypes a3d12e15) that had been hyperimmunized with Streptococcus pneumoniae (type III). In spite of the absence of either specific DNA probes for rabbit immunoglobulin (Ig) sequences or cross‐hybridizing mouse Ig DNA probes, recombinant clones containing cDNA sequences of rabbit γ heavy chain and x light chains were identified by a combination of screening techniques: (a) colony hybridization using labeled mRNA; (b) mRNA hybridization selection and translation and (c) hybridization to electrophoretically fractionated poly A(+)‐RNA (“Northern” analysis). Sequencing of three x light chain recombinant DNA sequences, including part of the 3′ untranslated (UT) region, has confirmed the fact that recombinant DNA for x light chain mRNA has been identified. An unexpectedly high degree of homology between the 3′ UT region sequence of this DNA from a rabbit of b5 allotype and the published 3′ UT sequence from a b4 rabbit was found. It appears that 3′ UT sequences from b4 and b5 alleles have diverged less than the coding sequences for the constant regions. The functional significance of this conservation of 3′ UT sequences remains to be elucidated.
Effect of cyclosporin A on spontaneous autoimmune thyroiditis of Obese strain (OS) chickens
Authors: Wick Georg , Müller Pia‐Ulrike , Schwarz Siegfried 
Published: February 2007

AbstractThe spontaneous autoimmune thyroiditis (SAT) which develops in the Obese strain (OS) of chickens depends on an intact B‐dependent portion of immune system. T helper cells have been shown to be required for the production of thyroglobulin autoantibodies (Tg‐AAb), but a possible contribution of cytotoxic T cells in the initial phases of SAT still remains to be elucidated. Cyclosporin A (CsA), an immunosuppressive drug with selective activity on T blast formation was used as a probe to clarify this issue: (a) the immunosuppressive potential of CsA was first verified for an avian species by demonstrating prolongation of skin allograft survival; (b) posthatching treatment of OS chickens with CsA until they were killed at 3 weeks of age did not alter the frequency and severity of SAT and the incidence and titer of Tg‐AAb; (c) treatment of OS embryos on days 15, 17 and 19 of incubation entailed the development of significantly more severe disease and higher titers of Tg‐AAb as compared to controls. A possible effect of CsA on precursors of suppressor T cells in the chicken is postulated. Cytotoxic T cells seem to play a minor role in the beginning of thyroid infiltration. It is concluded that CsA may not be the drug of choice for treatment of at least some autoimmune diseases.
Natural and antibody‐dependent killer cells in the thymus
Authors: Zöller Margot , Andrighetto Giancarlo , Heyman Birgitta 
Published: February 2007

AbstractThymocytes contain a small population of light (ϱ = 1.067), large cells with high cytolytic potential against natural killer target as well as against IgG‐ or IgM‐coated erythrocytes and nucleated cells, thus displaying natural killer and antibody‐dependent cellular cytotoxicity functions, but not exhibiting T killer cell capacity.As far as characterized, the cells show T cell characteristics: they are nonadherent, nonphagocytic, surface immunoglobulin‐negative, C3 receptor‐negative, partly Fey receptor‐positive, carry the receptor for Helix pomatia A agglutinin, and are, at least partly, cortisone‐resistant and Thy‐1‐positive.The implications of this finding with respect to the lineage of natural killer and killer cells and their interdependence will be discussed briefly.