bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trans Gene Complementation of I-E Subregion Antigens
Authors: Silver Jack 
Published: December 2022

Abstract
The murine I-E subregion antigens consist of two polypeptide chains designated α and β with m.w. of 32,000 and 29,000, respectively. These murine antigenic complexes can be precipitated with specific alloantiserum from mice possessing an I-E subregion derived from H-2 haplotypes k, d, p, or r (1–5). Other mice either do not express the I-E subregion antigen or have it in a serologically undetectable form (5–7). Although the appropriate I-E subregion (I-Ed, p, k, or r) is necessary for detection of I-E subregion antigens, the structural polymorphism of Eβ chains is determined by a gene outside the I-E subregion and within the K to I-B genetic interval of the major histocompatibility complex (MHC) (8–10). This observation was made after studies by Jones et al. (5) indicated that expression of I-E subregion antigens required two genes, one in the I-A subregion and the other in the I-E subregion, and suggested that this might explain why for some mice maximum immune responses require complementation by two genes, one in the I-A or I-B and the other in the I-E or I-C subregion.
Characterization of a Spontaneous Murine B Cell Leukemia (BCL1)
Authors: Knapp M. R. , Jones P. P. , Black S. J. , Vitetta E. S. , Slavin S. , Strober S. 
Published: December 2022

Abstract
The surface marker expression of a spontaneous B lymphocyte leukemia discovered in a BALB/c mouse (BCL1) was examined and found to include a subset of markers known to occur on normal B lymphocytes. The tumor cells bore surface Ig that included both µ- and δ-chains associated with the λ light chain. Alloantigens coded for within the murine MHC, including H-2D, H-2K, and I-region products, were identified on the tumor cells. Although normal B lymphocytes are thought to express products coded for within both the I-A and I-E subregions, the BCL1 expressed only normal amounts of I-E subregion products. In addition, the H-2 and Ia antigens revealed by 2-dimensional gel electrophoresis exhibited an abnormal pattern of post-translational modifications. The Fc, but not the complement-receptor, was present on the surface of tumor cells. The presence of IgD, Ia antigens, and the responsiveness to lipopolysaccharide (see subsequent paper) have led us to postulate that the BCL1 tumor represents a later differentiative stage than murine B lymphocyte tumors previously described.
Heterogeneity of Binding of Human IgA Subclasses to Protein A
Authors: Brunda Michael J. , Minden Percy , Grey Howard M. 
Published: December 2022

Abstract
The ability of human IgA myeloma immunoglobulins to interact with protein A-containing Staphylococcus aureus was examined. Some IgA1 and IgA2 immunoglobulins bound to S. aureus although others of both subclasses failed to do so. These results were obtained by using both direct binding of radiolabeled immunoglobulins to S. aureus and with inhibition-type assays. Binding was dependent on the Fc fragment of IgA since there was no binding to S. aureus by an F(ab′)2 fragment of IgA1. Nonprotein A-containing bacteria did not bind these immunoglobulins and isolated protein A interacted with radiolabeled immunoglobulins. This strongly suggested that protein A was responsible for the observed binding to S. aureus. These data indicate, in contrast to previous reports, that there is no simple relationship between IgA subclass and the capacity to bind to protein A.
Biologic Activity of Rabbit Antisera Directed against in Vitro Stimulated Guinea Pig T Lymphocytes
Authors: Thomas David W. , Meltz Susan K. , Hahn Yaffa , Schwartz Benjamin D. 
Published: December 2022

Abstract
In this communication we examined the functional activity of rabbit antisera produced against guinea pig T lymphocytes that had been stimulated in vitro by culture with macrophage-associated antigen. One antiserum (96-2) was raised against strain 13 T cells that were primed by culture for a week with trinitrophenyl-(TNP) modified syngeneic macrophages. Addition of 96-2 serum to TNP-primed strain 13 T cells or strain 13 T cells primed in a mixed leukocyte reaction (MLR) stimulated a dramatic increase in DNA synthesis in vitro. In contrast, strain 13 T cells primed in vitro with several protein antigens failed to be stimulated by the 96-2 serum. In addition, 96-2 serum produced little stimulation of TNP or MLR-primed strain 2 cells, or of strain 13 T cells taken directly from the animal. Another antiserum (144-2) was raised against glutamic acid-lysine copolymer (GL)-immune strain 2 T cells selected by culture with GL-pulsed strain 2 macrophages. Addition of 144-2 serum to GL-selected or MLR-primed strain 2 T cells also produced a dramatic proliferative response. However, 144-2 serum did not stimulate TNP-primed strain 2 or strain 13 T cells, or strain 2 T cells selected with unrelated protein antigens. By several techniques we showed that contaminating B cells in the primed T cell preparations were not responsible for the observed proliferation and that the antisera directly stimulated highly purified T cells. The proliferative activity of 96-2 and 144-2 could be removed by absorption with nonimmune spleen cells. Physicochemical analysis of the cellular antigens detected by the antisera showed molecular species of 98,000, 70,000, 33,000 and 25,000 daltons. By sequential immunoprecipitation analyses, the latter two peaks were determined to be Ia antigens, the 70,000 peak of in vitro primed cells contained some immunoglobulin-like molecules and another nonimmunoglobulin-like antigenic species, and the 98,000 species appeared unrelated to immunoglobulin or Ia antigens.
Regulation of Contact Sensitivity to Dnfb in the Mouse: Effects of Adult Thymectomy and Thymic Factor
Authors: Erard D. , Charreire J. , Auffredou M. T. , Galanaud P. , Bach J. F. 
Published: December 2022

Abstract
The contact sensitivity response to DNFB is decreased after adult thymectomy (ATX). This response decreases to 50% of the control response of normal age-matched mice as soon as 3 weeks after ATX and is not further depressed 9 to 16 weeks after ATX. These results suggest that two T cell subsets of different lifespan are involved in the anti-DNFB response. A circulating thymic factor (FTS) is able to restore the contact sensitivity response to DNFB when injected 3 to 9 weeks after ATX but not 16 weeks later. By contrast, FTS has a depressive effect on the contact sensitivity response to DNFB of normal mice through a cyclophosphamide-sensitive T cell subset. These results suggest that FTS regulates DNFB contact sensitivity by acting on a cyclophosphamide-sensitive T cell subset, still present 9 weeks after ATX but absent after 16 weeks. Thus although the T cell defect, causing a depression of the contact sensitivity reaction to DNFB is quantitatively similar 3 and 16 weeks after ATX, its nature is probably different.
Studies of Reticuloendothelial Function in the Mouse with Model Immune Complexes
Authors: Finbloom David S. , Plotz Paul H. 
Published: December 2022

Abstract
We have extended the findings in the accompanying paper by characterizing the serum clearance and tissue uptake of model soluble immune complexes and the saturation of the reticuloendothelial system (RES) by these complexes in normal mice and in mice with murine lupus (NZB/W F1 females). Adult NZB/W or young C3H mice were injected with radiolabeled stable site-specifically cross-linked mouse anti-DNP oligomers as model immune complexes to proble RES function. Blood clearance and uptake by liver, spleen, and kidney were unimpaired in NZB/W mice. To determine if the RES exhibits partial saturation in the NZB/W mice, we deliberately induced a state of RES blockade with heat-aggregated human γ-glubulin (HAG). With increasing doses of HAG (1 to 4 mg/20 g body weight) both strains similarly showed a progressive increase in RES saturation as measured by reduced liver upake of model oligomers. Recovery from saturation was complete by 120 min in both strains. At maximal liver saturation there was only a small increase in oligomer uptake by kidney or spleen, the majority of complexes remaining within the circulation. Thus, RES capacity for handling soluble model immune complexes appears unimpaired in NZB/W mice.
Glucocorticoid-Induced Inhibition of T Cell Growth Factor Production
Authors: Gillis Steven , Crabtree Gerald R. , Smith Kendall A. 
Published: December 2022

Abstract
The previous communication presented data detailing that glucocorticoid hormones exhibited slight but significant inhibitory effects on the proliferation of cytolytic T cells maintained in long-term T cell growth factor (TCGF)-dependent cultures. However, most importantly, glucocorticoids were shown to inhibit T-lymphocyte proliferation via a profound effect on TCGF production. Addition of exogenous TCGF to glucocorticoid-treated human, mouse, or rat T cell mitogen-stimulated lymphocytes restored normal levels of proliferation. These observations led us to propose that the immunosuppressive effects of glucocorticoid hormones were mediated by controlling the production of the T cell proliferation-inducing agent, TCGF.
Results of experimentation detailed in this communication provide further evidence in support of this hypothesis. We found that although glucocorticoid hormones had little effect on the cytolytic reactivity of T cells harvested from TCGF-dependent culture, treatment of mixed lymphocyte cultures (MLC) with identical glucocorticoid hormone concentrations completely abrogated in situ TCGF production and alloantigen-directed cytolysis. The inhibitory effects of glucocorticoids in MLC could be eliminated once again simply by the delayed addition of exogenous TCGF. These observations coupled with those detailed in the previous report provide evidence that, rather than effecting lysis of potentially reactive mature lymphocytes, glucocorticoids influence the development of T cell-mediated immune reactivity by inhibiting TCGF production, which in turn serves to inhibit the clonal expansion of activated T cells.
Tissue Distribution of Immunoglobulin-Secreting Cells in Normal and IgA-Deficient Chickens
Authors: Clinton Lawrence E. , Arnaud-Battandier Franck , Koski Irma R. , Dooley Nancy J. , Muchmore Andrew V. , Michael Blaese R. 
Published: December 2022

Abstract
A reverse hemolytic plaque assay was employed to enumerate lymphoid cells actively secreting either immunoglobulin (Ig)G, IgA, or IgM in the small intestine, lungs, and lymphoid organs of normal and IgA-deficient chickens. In normal birds, intestinal lamina propria lymphocytes were proportionately richest in cells secreting IgG and IgA whereas the bone marrow was richest in IgM-secreting cells. The highest ratio of IgA to IgG secreting cells was also found in the lamina propria lymphocytes of the intestine (0.9), followed by the IgA to IgG ratios in the intestinal epithelium (0.31), and the lungs (0.19). The IgA to IgG ratios in the bone marrow (0.08) and the spleen (0.02) were considerably lower. Thus, both the intestine and the lungs were relatively enriched in cells actively secreting IgA. These IgA-secreting cells are the likely source of the IgA found in such quantities in intestinal and respiratory secretions.
The tissue distribution of Ig-secreting cells was also studied in two generations of birds with experimentally induced IgA deficiency. There was a striking diminution of IgA-secreting cells in all tissues, including the intestine and lungs, whereas cells secreting IgG and IgM were normal or increased. The lack of IgA-secreting cells in these birds represents the effects of donor suppressor T cells having specificity for IgA.
Human IgE Biosynthesis in Vitro: Studies with Atopic and Normal Blood Mononuclear Cells and Subpopulations
Authors: Fiser Paul Martin , Buckley Rebecca H. 
Published: December 2022

Abstract
IgE synthesis was investigated in cultures of unfractionated human blood mononuclear cells and of T- and B-enriched subpopulations. The facts that IgE released from initial cell pellets by a pH 3.7 buffer or freezing and thawing was much smaller in amount than in 7-day supernatants and that IgE production was markedly inhibited by puromycin and/or mitomycin C provided evidence for synthesis. The geometric means of PWM-stimulated and unstimulated IgE synthesis did not differ statistically. Unfractionated and B-enriched cells from 15 atopic donors with elevated serum IgE made significantly more IgE than did those from normals (p = &lt;0.0001). Co-cultures of patient and control unstimulated and unfractionated cells produced less IgE than expected for 11 of 15 patients, with the overall geometric mean being 62% less (p = &lt;0.05). B cells from some patients showed marked augmentation of IgE synthesis, suggesting that autologous T cells had had some suppressive effect. Assays of the same B cell supernatants for IgM failed to show similar augmentation. This observation and the finding of IgE production by unstimulated cells suggest that the IgE synthesis may have been stimulated in vivo. Recombinations of T and B cells revealed a greater tendency for T cells from normals to suppress IgE synthesis by patient B cells than did autologous T cells (p = NS). These data support the possibility that atopics have a relative deficiency of a regulatory cell or function that in normals prevents excessive IgE production. The fact that co-culturing patient T with normal B cells did not markedly increase IgE synthesis suggests that differences between normals and atopics involve both the T and the B subpopulations.
Measurement of Cell-Mediated Inflammation in Experimental Murine Autoimmune Encephalomyelitis by Radioisotopic Labeling
Authors: Scott Linthicum D. , Mackay Ian R. , Carnegie Patrick R. 
Published: December 2022

Abstract
A radioisotopic index test was used to detect that time of onset and intensity of cell-mediated immune inflammation of experimental autoimmune encephalomyelitis (EAE) in mice. Mice were tested at various time intervals after an encephalitogenic immunization with mouse spinal cord homogenate for delayed-type hypersensitivity (DTH) to myelin basic protein (MBP) by intradermal challenge with antigen in the ear pinna. After 24 hr, the intensity of DTH was measured by 125I-radiometry which depends upon the migration of 125I-UdR radiolabeled mononuclear cells into the antigen depot. Cells reactive to MBP were detected by the ear assay as early as 7 days after the initial encephalitogenic sensitization. The degree of cell-mediated immune inflammation in the brain and spinal cord during the evolution of EAE was also measured by a radioisotopic technique; increased 125I-UdR uptake could be detected in the brain 3 to 4 days before the onset of signs of EAE at days 11 to 12, whereas 125I-UdR in the spinal cord was detected only 1 day before, or concomitant with, the onset of signs of EAE. Both the “ear” and “organ” radiometric index tests are useful in measuring the degree of cell-mediated inflammation in EAE, and supplement routine histopathological and observational assessments.
Effector mechanisms of cytolytically activated macrophages. I. Secretion of neutral proteases and effect of protease inhibitors.
Authors: Adams D O 
Published: December 2022

Abstract
Peritoneal macrophages from C56BL/6J mice, when activated by bacillus Calmette-Guérin, lysed syngeneic MCA-I sarcoma targets but not syngeneic embryo fibroblasts. Inflammatory macrophages elicited by concanavalin A (Con A) did not appreciably lyse either target. The activated macrophages secreted more neutral proteases into the extracellular compartment, both absolutely and relative to intracellular content, than did the Con A inflammatory macrophages. Bovine pancreatic trypsin inhibitor (BPTI) (750 KIU/ml) and diisopropylfluorophosphate (2 x 10(-3) M) inhibited cytolysis of neoplastic targets by the activated macrophages. The BPTI had to be present during the 48-hr macrophage-tumor cell interaction to reduce cytolysis; pretreatment of either the macrophages or the targets by the BPTI did not reduce cytolysis. The inhibitors, at the concentrations found to inhibit cytolysis, were not toxic to the macrophages as judged by morphology, by the ability of the macrophages to incorporate leucine into protein, and by the potential for cytolytic activation of the macrophages in vitro. It is suggested that neutral serine protease(s) secreted by activated macrophages participate in the cytolytic destruction of neoplastic cells.
Complement receptors on guinea pig epidermal Langerhans cells.
Authors: Berman B , Gigli I 
Published: December 2022

Abstract
A population of guinea pig epidermal cells possessed the ability to form rosettes with IgM antibody-sensitized sheep erythrocytes coated with purified human C3b (SEAIgMC1-), but not with intermediates carrying C1, C4, or C2. This population of rosette-forming epidermal cells was identified as Langerhans cells (LC) ultrastructurally and by LC depletion and enrichment studies. In addition, these cells were able to bind fluid phase C3b, which inhibited any subsequent SEAIgMC1-3b rosette formation. Rosette formation was also inhibited after SEAIgMC1-3b pretreatment with beta 1H and C3b-inactivator. LC were shown to possess trypsin-resistant C3b and Fc receptors, and unlike the temperature-independent nature of LC Fc-rosette formation, the ability of LC to form C3 rosettes was a temperature-dependent process. The finding of C3b receptors on the surface of guinea pig epidermal LC supports the concept that they are of the phagocytic monocyte-macrophage family.
The effects of dialyzable products from human leukocyte extracts on cutaneous delayed-hypersensitivity response.
Authors: Gottlieb A A , Maziarz G A , Tamaki N , Sutcliffe S B 
Published: December 2022

Abstract
Fractions from human whole leukocyte lysates were prepared by sequential double dialysis against membranes with cut-offs of m.w. 12,000 and 3500, and by elution chromatography on Sephadex G-10. The effect of localized intracutaneous implantation of fractions with m.w. less than 3500 was studied. Two types of response were obtained: 1) the amplification of response to antigen to which the donor had preexisting immunity, and 2) the induction of inflammatory response histologically resembling delayed hypersensitivity in the absence of added antigen. The substances mediating these responses could be separated into unique components by use of a long (1 x 150 cm) G-10 column, or by hydroxylapatite chromatography. The active principles were derived from leukocyte extracts (as demonstrated by their absence from autologous RBC extracts prepared by identical methodology), and the histopathologic appearances after intracutaneous implantation were compatible with those of a delayed-hypersensitivity response. No evidence of transfer of antigen-specific information from a sensitive donor to a nonsensitive recipient was obtained under the conditions of study.
Mitogenic effect on human lymphocytes of insolubilized anti-immunoglobulins. I. Specificity of the stimulating agent.
Authors: Henriksen A , Godal T , Landaas T O 
Published: December 2022

Abstract
The mitogenic response of peripheral blood lymphocytes to various anti-immunoglobulin reagents has been studied by measuring incorporation of a radioactive thymidine into macromolecules. Coupling of anti-F(ab')2 or anti-light chain antibodies to Sepharose beads leads to a 5-fold increase in their mitogenic capacity with 50-fold less antibodies per culture. Pepsin-digested F(ab')2 fragments had a mitogenic capacity similar to intact antibody molecules. Anti-F(ab')2 antibodies purified by immunoabsorbent columns were found to be more effective as mitogen than unpurified antibody fractions. Antibodies to kappa- or lambda-light chains were found to be mitogenic, whereas antibodies specific to various heavy chain classes failed to induce a significant response. Isolated light chains were much more effective in inhibiting the reaction than isolated mu-chains. It is concluded that insolubilized anti-light chain antibodies are mitogenic to human peripheral blood lymphocytes.
Control of autologous immune complex nephritis. I. Suppression of the disease in the presence of T cell sensitization.
Authors: Harmon W E , Grupe W E , Parkman R 
Published: December 2022

Abstract
Pretreatment of Lewis and Sprague-Dawley rats with the nephritogenic antigen, Fx1A, in incomplete Freund's adjuvant (IFA) reduced the incidence of autologous immune complex nephritis in rats subsequently challenged with Fx1A in complete Freund's adjuvant (CFA). The suppression was evidenced by a decrease in antibody production, in glomerular deposition of immunoglobulins, and in the incidence of proteinuria, and it was antigen specific. In vitro blastogenesis to Fx1A of lymphocytes from Fx1A-IFA-pretreated animals was normal. Rats pretreated with Fx1A-IFA initially developed a normal antibody response after challenge with Fx1A-CFA, but the response was not sustained. These results indicate that the Fx1A-IFA-induced suppressor mechanism does not inhibit sensitization, but rather modifies specific antibody production.
Serum antibodies to human fetal antigens in patients with systemic lupus erythematosus (SLE).
Authors: Linker-Israeli M , Quismorio F P , Wong D K , Friou G J 
Published: December 2022

Abstract
Serum antibodies to human fetal antigens were measured by a radiolabeled anti-immunoglobulin binding assay by using human fetal fibroblasts (Flow cell line No. 1000) as target cells. High titers of IgG antibody to the fetal cells were found in sera of patients with systemic lupus erythematosus (SLE). The antibody reacted with surface membrane antigens shared by various fetal tissues of human and murine origin but not by adult tissues. The reaction of the SLE antibody to the fetal cells was inhibited by heterologous antiserum to the Flow 1000 cells and antiserum to murine embryonic fibroblasts, but not by antiserum to human alpha-fetoprotein or human fibronectin. Absorption of SLE serum with isolated nuclei did not abolish the reaction indicating that these were not anti-nuclear antibodies. The antibody activity was found to reside in the F(ab')2 fragment. The serum titer of the anti-fetal antibody was higher in SLE patients with active disease than those in clinical remission.
Reduced natural killer activity in female mice after neonatal exposure to diethylstilbestrol.
Authors: Kalland T 
Published: December 2022

Abstract
Treatment of neonatal female mice with DES markedly reduced the activity of NK cells in adult mice. This finding was most evident in C57BL/6 and BALB/c strains, but was also found in outbred NMRI mice. The mechanisms behind the reduced NK activity was further analyzed. No evidence of DES-induced cellular or humoral suppressors of natural killing could be detected. Pregnancy was found to be without effects on NK. Poly I:C augmented the NK activity in control females but even very high doses of Poly I:C failed to increase the level of NK activity in neonatally DES-treated animals. The lack of response to boosting with Poly I:C was not due to alterations in kinetics of NK induction.