bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of BSF-2/IL-6 production by human mononuclear cells. Macrophage-dependent synthesis of BSF-2/IL-6 by T cells.
Authors: Horii Y , Muraguchi A , Suematsu S , Matsuda T , Yoshizaki K , Hirano T , Kishimoto T 
Published: December 2022

Abstract
Regulation of BSF-2/IL-6 production in peripheral mononuclear cells (MNC) was studied. BSF-2 mRNA expression in mitogen-stimulated MNC showed a biphasic response, the first peak around 4 h and the second peak around 48 h. This was caused by different kinetics of BSF-2 mRNA expression in distinct subpopulations of MNC; M phi expressed BSF-2 mRNA at 5 h in the absence of any stimulation, and mitogen-stimulated T cells and B cells expressed BSF-2 mRNA 48 h after stimulation. Immunohistochemical staining of the cells with anti-BSF-2 antibody demonstrated that macrophages, T cells and B cells could produce BSF-2. T cells in peripheral MNC produced BSF-2 in the presence of M phi. The requirement of macrophage for BSF-2 production in T cells could be replaced by TPA but not by IL-1 or BSF-2.
Characterization of higher avidity monoclonal antibodies produced by murine B-cell hybridoma variants selected for increased antigen binding of membrane Ig.
Authors: Martel F , Bazin R , Verrette S , Lemieux R 
Published: December 2022

Abstract
Somatic mutation in the Ig genes plays a major role in the increase of antibody affinity observed in secondary immunologic responses. It has been shown that the mechanism responsible for the high rate of somatic mutation in the Ig genes was active not only in normal B lymphocytes but also in B-cell hybridomas secreting mAb. Also, it has been reported that B-cell hybridomas were positive for membrane Ig of the same specificity as the secreted mAb. The presence of membrane Ig suggested that somatic variants secreting mAb of higher affinity could be selected by the increased capacity of these hybridoma cells to bind immobilized Ag. This hypothesis was tested with hybridoma cells secreting an IgM mAb reacting with the A Ag of the ABO blood group system. In two selection experiments, we have isolated several variant cell lines secreting mAb of increased avidity for the A Ag under similar IgM concentrations. Biochemical characterization of one of the variant mAb indicated that the mutation responsible for the increased avidity has occurred in the heavy chain gene. The method developed may have profound implications for the diagnostic and therapeutic use of mAb and will permit the study, in an in vitro system, of the role of somatic mutations in antibody diversity.
Effect of cytokines on polymorphonuclear neutrophil infiltration in the mouse. Prostaglandin- and leukotriene-independent induction of infiltration by IL-1 and tumor necrosis factor.
Authors: Sayers T J , Wiltrout T A , Bull C A , Denn A C , Pilaro A M , Lokesh B 
Published: December 2022

Abstract
The i.p. injection of mice with highly purified recombinant human rIL-1 alpha or beta resulted in the rapid influx of a large number of polymorphonuclear neutrophils (PMN) into the peritoneal cavity. Significant increases in the number of PMN were induced by doses of IL-1 which ranged from 0.005 to 5 ng/injection. Interestingly the dose response for PMN influx was bell-shaped because 50 ng of IL-1 did not result in a significant increase in peritoneal PMN. IL-1 induced PMN infiltration was detectable by 1 h with peak levels of PMN obtained by about 2 h, followed by a subsequent decline by 24 h. Other cytokines, IL-2, IFN-gamma, IFN alpha beta, granulocyte-CSF, granulocyte-macrophage-CSF, IL-3, TNF-alpha, and TNF-beta were compared to IL-1 for their ability to induce a PMN influx into the peritoneum. Only TNF-alpha or TNF-beta (lymphotoxin) were able to induce a significant influx of PMN within 2 h. However, based on total protein administered, about 100 times more TNF than IL-1 was required to produce a comparable PMN infiltration. Intraperitoneal injection of inhibitors of the cyclooxygenase or lipoxygenase pathways did not inhibit the IL-1-induced influx of PMN. Also, neither IL-1 nor TNF triggered an increase in PG or leukotriene release from peritoneal cells in vitro. Furthermore, direct peritoneal injection of leukotriene B4, a potent PMN chemoattractant in vitro, did not induce any significant increase in PMN in the peritoneal cavity indicating that chemotactic activity alone is insufficient for inducing peritoneal infiltration. These results suggest that the local production of very low levels of IL-1 in vivo would be sufficient to initiate a sequence of events that results in a rapid accumulation of PMN. Because IL-1 was not chemotactic for PMN in vitro, our data suggest that IL-1 induces production of factors that are chemotactic for PMN. Alternatively, IL-1 may act on other stages of the complex sequence of events that regulates the emigration of PMN into tissue sites in vivo. The synergy apparent in PMN influx when suboptimal concentrations of IL-1 and TNF were injected suggests that the local production of very low concentrations of these cytokines in situ could play a critical role in the emigration of PMN during infection.
The molecular basis of granuloma formation in schistosomiasis. I. A T cell-derived suppressor effector factor.
Authors: Perrin P J , Phillips S M 
Published: December 2022

Abstract
These studies define certain T cell-dependent regulatory factors that modulate granulomatous hypersensitivity in Schistosoma mansoni. Lyt-2+ and IJ+ T cells produce a suppressor effector factor (TseF) that bears both an IJ determinant and an antigenically specific receptor. TseF suppresses in vitro and in vivo granulomatous hypersensitivity and demonstrates both antigenic and genetic restriction. This factor binds to the mAb 14-12 but not 14-30 suggesting that it also bears a specific suppressor effector phenotypic marker. Factor production is abrogated by the addition of exogenous IL-2; however, the activity of preformed TseF is not affected by IL-2. Initial characterization studies have suggested that TseF is a non-Ig protein and that it is composed of two chains that can be separated by dithiothreitol reduction. These chains can complement each other by in vitro reconstitution of reactivity. One chain bears the IJ phenotype. The other chain bears the Ag-R. Thus it would appear that this TseF bears strong structural homologies to those previously ascribed to T cell-R. These studies provide preliminary information on the molecules that are responsible for the specific modulation of granulomatous hypersensitivity in schistosomiasis.
Cloned and expressed human Fc receptor for IgG mediates anti-CD3-dependent lymphoproliferation.
Authors: Peltz G A , Trounstine M L , Moore K W 
Published: December 2022

Abstract
We have utilized gene transfer experiments to investigate the role of a human monocyte receptor for IgG (Fc gamma RII) in mouse IgG1 anti-CD3 (Leu 4)-induced lymphoproliferation in vitro. Mouse Ltk- cells expressing human Fc gamma RII or a mutant of Fc gamma RII lacking the entire cytoplasmic domain of the receptor mediate anti-CD3-induced lymphoproliferation in cultures of adherent cell-depleted human PBMC. Expression of an Fc gamma RII mutant lacking transmembrane and cytoplasmic domains (soluble Fc gamma RII) in COS7 cells yielded a secreted receptor which retained affinity for IgG, even in the absence of the mutant receptor's N-linked oligosaccharides. Soluble Fc gamma RII inhibits rosette formation by human IgG-sensitized RBC and the Fc gamma RII-bearing cell line K562, but does not sitmulate anti-CD3-induced lymphoproliferation under the conditions tested.
T cell antigen receptors in autoimmunity.
Authors: Posnett D N , Gottlieb A , Bussel J B , Friedman S M , Chiorazzi N , Li Y , Szabo P , Farid N R , Robinson M A 
Published: December 2022

Abstract
Three mAb to variable region determinants of the alpha/beta-chain TCR were used to detect discrete populations of peripheral blood T cells. T cells sharing a TCR determinant defined by such an antibody presumably use the same or similar TCR V or J genes for their alpha- or beta-chains. Thus analysis with these mAb provides a tool to investigate TCR gene usage and expression. Since autoantigen specific T cells may play an important role in initiating autoimmune diseases, TCR were analyzed in different autoimmune diseases and control groups including rheumatoid arthritis, Graves disease, idiopathic thrombocytopenic purpura, psoriasis, SLE, insulin-dependent diabetes mellitus, and in nonautoimmune control diseases and normals. Purified T cells were stained by indirect immunofluorescence with three mAb to TCR variable regions: mAb S511 stains 1.8 +/- 0.9% (mean +/- 2 SD), mAb C37 stains 3.4 +/- 1.5% and mAb OT145 stains from 0 to 6% of T cells from normal donors. Several individuals were identified with expanded subsets of positive T cells. One patient with adult ITP followed during a 12-mo period consistently had elevated percentages of T cells staining with the mAb OT145 (15.9 to 24.5%). These cells were found to be exclusively CD8+. By Southern blotting DNA prepared from these OT145+, CD8+ cells, but not DNA from the patient's OT145- T cells, revealed a clonal rearrangement using a beta-chain C region probe. Thus this patient had a monoclonal expansion of CD8+, OT145+ cells. Hyperexpression of a TCR variable region, as defined by the available mAb, could not be associated with any of the diseases studied. Examination of T cells at the site of autoimmunity, such as T cells from rheumatoid arthritis synovial fluid, revealed normal percentages of cells staining with these mAb. Immunoperoxidase staining of psoriatic lesional skin showed no striking enrichment of T cells bearing one or the other TCR type.
Plasmacytoma growth factor activity of murine granulocyte-macrophage colony-stimulating factor.
Authors: Vink A , Vandenabeele P , Uyttenhove C , Cayphas S , Van Snick J 
Published: December 2022

Abstract
Mouse plasmacytoma FLOPC21 was adapted to culture in the presence of a mouse Th cell supernatant. A stable factor-dependent cell line was derived from this culture and the factor responsible for its growth was identified as granulocyte-macrophage colony-stimulating factor.
Human recombinant IL-4 induces activated B lymphocytes to produce IgG and IgM.
Authors: Defrance T , Vanbervliet B , Pène J , Banchereau J 
Published: December 2022

Abstract
In this report, we describe a novel biologic activity of IL-4 namely, its ability to induce activated human B cells to produce IgM. Staphylococcus aureus Cowan I-activated blasts prepared from high density tonsil B cells were found to secrete IgG and IgM, but no IgE, when cultured in the presence of rIL-4. The differentiating activity of rIL-4 was totally blocked by a neutralizing anti-IL-4 antiserum, therefore demonstrating that the IgG/IgM-inducing activity of rIL-4 was an intrinsic property of IL-4. rIL-4 was only minimally inducing Ig production of blasts prepared from low density B cells, whereas it induced B cell blasts prepared from high density B cells to secrete a high amount of Ig. Delayed additions of the neutralizing anti-IL-4 antiserum demonstrated that a 48-h contact between IL-4 and B cell blasts was required for optimal Ig production. The IL-4-mediated IgG and IgM production was neither suppressed by IFN-gamma nor by anti-CD23 mAb 25, whereas these agents have been shown earlier to inhibit IgE production of enriched B cells cultured in the presence of IL-4. These data indicate that the IgG/IgM-inducing activity of IL-4 is not regulated like the IL-4-induced IgE production by enriched B cells.
A novel IFN-gamma regulated human melanoma associated antigen gp33-38 defined by monoclonal antibody Me14/D12. I. Identification and immunochemical characterization.
Authors: Giuffré L , Isler P , Mach J P , Carrel S 
Published: December 2022

Abstract
A novel melanoma-associated differentiation Ag whose surface expression can be enhanced or induced by IFN-gamma was identified by mAb Me14/D12. Testing of numerous tumor cell lines and tumor tissue sections showed that Me14/D12-defined Ag was present not only on melanoma but also on other tumor lines of neuroectodermal origin such as gliomas and neuroblastomas and on some lymphoblastic B cell lines, on monocytes and macrophages. Immunoprecipitation by mAb Me14/D12 of lysates from [35S]methionine-labeled melanoma cells analyzed by SDS-PAGE revealed two polypeptide chains of 33 and 38 KDa, both under reducing and nonreducing conditions. Cross-linking experiments indicated that the two chains were present at the cell surface as a dimeric structure. Two-dimensional gel electrophoresis showed that the two chains of 33 and 38 KDa had isoelectric points of 6.2 and 5.7, respectively. Treatment of the melanoma cells with tunicamycin, an inhibitor of N-linked glycosylation, resulted in a reduction of the Mr from 33 to 24 KDa and from 38 to 26 KDa. Peptide maps obtained after Staphylococcus aureus V8 protease digestion showed no shared peptides between the two chains. Although biochemical data indicate that Me14/D12 molecules do not correspond to any known MHC class II Ag, their dimeric structure, tissue distribution, and regulation of IFN-gamma suggest that they could represent a new member of the MHC class II family.
Functional differences between the 40 kDa and 50 to 70 kDa IgG Fc receptors on human neutrophils revealed by elastase treatment and antireceptor antibodies.
Authors: Tosi M F , Berger M 
Published: December 2022

Abstract
Most previous studies of IgG FcR on neutrophils (PMN) have focused on a single FcR of Mr = 50 to 70 kDa, which is recognized by mAb 3G8 and anti-Leu-11a. In the course of studying the effects of extracellular proteases on PMN receptor expression and function, we found that treatment with human leukocyte elastase reduced the expression of this FcR on the PMN surface by as much as 85% in flow cytometric studies, but did not inhibit ingestion of IgG-coated particles or O2- production induced by multivalent IgG complexes, and caused only a 35% decrease in IC binding to PMN. Since a second FcR with Mr = 40 kDa recognized by mAb IV-3, recently has been identified on PMN, we sought to determine if this FcR was resistant to elastase and thus accounted for the elastase stability of IgG-mediated PMN functions. Elastase treatment that reduced 3G8 binding by 85% caused no decrease in binding of mAb IV-3. For non-elastase-treated PMN, mAb IV-3 against the 40 kDa FcR caused as much as 79 +/- 7% inhibition of IgG-induced O2- production, whereas mAb 3G8 against the 50 to 70 kDa FcR caused only 32 +/- 5% inhibition. In contrast, for IC-binding, mAb IV-3 caused only 15 +/- 6% inhibition, whereas mAb 3G8 caused as much as 80 +/- 9% inhibition, a reversal of their relative effects on O2- production. In parallel studies with elastase-treated PMN, mAb IV-3 actually blocked more IC binding than did mAb 3G8, 55 +/- 4% vs 40 +/- 6%, respectively, presumably because most of the 50 to 70 kDa FcR molecules had been cleaved. The effect of the two mAb together in blocking IC binding was additive, whereas for blocking of O2- production, mAb 3G8 added little or nothing to the effect of mAb IV-3 alone. Direct 125I-labeled Ab binding studies with intact PMN revealed seven times as many 50 to 70 kDa as 40kDa FcR, 110,200 +/- 9600 and 15,100 +/- 700 sites/cell, respectively. Our findings suggest that the elastase-resistant 40 kDa FcR is primarily responsible for IgG-mediated activation of human PMN, whereas the elastase-sensitive 50 to 70 kDa FcR predominates in IC binding, by virtue of its numerical superiority, but does not directly activate the cell. The latter may serve to hold IgG-coated microorganisms or other multivalent IC in place at the PMN surface, enhancing contact with the 40 kDa FcR and thus facilitating cell activation in a cooperative manner.
Igh-C allotype-linked control of anti-DNA production and clonotype expression in mice infected with Plasmodium yoelii.
Authors: Yoshida H , Fossati L , Yoshida M , Abdelmoula M , Herrera S , Merino J , Lambert P H , Izui S 
Published: December 2022

Abstract
The infection of nonlethal strain of Plasmodium yoelii induces the formation of IgG anti-DNA antibodies as a result of polyclonal B cell activation. By using various nonautoimmune strains of mice including H-2 or Igh congenic or recombinant mice, the levels and clonotypes of anti-DNA antibodies elicited by the malaria infection were analyzed in relation to the expression of the MHC or Igh gene. Our results showed there were little, if any, differences in serum anti-DNA levels and their clonotypes among B10 and B6 H-2 congenic mice. In contrast, malaria-induced IgG anti-DNA responses markedly differed quantitatively and clonotypically between murine strains bearing the Ighb allotype and those bearing the Igha, Ighj, Ighd, or Ighn allotype. The latter group of mice produced approximately 5 to 10 times more IgG anti-DNA antibodies than the former group of mice. Clonotypically, mice bearing the Ighb allotype developed high alkaline anti-DNA antibodies of pH 8.0 to 8.5, whereas non-Ighb mice failed to express such alkaline anti-DNA spectrotypes, and exhibited more neutral spectrotypes (pH 7.0 to 8.0). Studies on the Igh recombinant mice indicated that the observed quantitative and clonotypical differences in IgG anti-DNA production was not associated with the variable region, but with the constant region of the Igh gene complex. Our results have suggested that IgG anti-DNA responses occurring as a result of polyclonal B cell activation during the course of malaria infection markedly differs quantitatively and clonotypically among murine strains and appear to be controlled at least in part by the Igh-C gene or gene(s) closely linked to it.
Isolation of protective T cells from BALB/cJ mice chronically infected with Leishmania donovani.
Authors: Holaday B , Sadick M D , Pearson R D 
Published: December 2022

Abstract
BALB/cJ mice, which are homozygous for Lshs on chromosone 1, are genetically susceptible to Leishmania donovani (S3), but spontaneously reduce their parasite burdens late in the course of infection. Spleens from chronically infected mice (5 to 8 mo) were found to have T cells that responded to leishmanial Ag by proliferating and secreting immune IFN. An IFN-secreting T cell line derived from the spleen of a chronically infected mouse, after boosting with leishmanial Ag and treatment with Pentostam to kill residual parasites, was able to activate macrophages to kill amastigotes in vitro. Furthermore, after adoptive transfer of this cell line, naive BALB/cJ mice challenged with amastigotes demonstrated a 42-fold reduction in parasite burden compared to controls. Four of five clones derived from the protective T cell line secreted IFN and proliferated between days 7 and 14 after Ag stimulation. All clones were Ly1+2-, L3T4+. Another T cell line, which had Ly1+2-, L3T4+ phenotype, was derived from the lymph nodes of s.c. immunized, uninfected mice. It multipled but never produced IFN in response to leishmanial Ag and failed to protect macrophages against L. donovani infection in vitro or in vivo. This nonprotective T cell line and the fifth clone from the protective line, which also did not secrete IFN, proliferated between days 2 and 7 after Ag stimulation. In summary, leishmania-responsive helper/inducer T cells, which produced IFN but were slow to proliferate in response to Ag in vitro and which were able to activate macrophages to reduce amastigotes in vitro and in vivo, are present in chronically infected BALB/cJ mice and may mediate the decrease in parasite burden during chronic infection.
Analysis of the molecular specificities of anti-class II monoclonal antibodies by using L cell transfectants expressing HLA class II molecules.
Authors: Klohe E P , Watts R , Bahl M , Alber C , Yu W Y , Anderson R , Silver J , Gregersen P K , Karr R W 
Published: December 2022

Abstract
Expressible HLA class II alpha- and beta-chain cDNA were used for DNA-mediated gene transfer to produce L cell transfectants expressing single types of human class II molecules. Cloned transfectants expressing nine different class II molecules were isolated: DR alpha: DR1 beta I, DR alpha: DR4 beta I, DR alpha: DR5 beta I, DR alpha: DR5 beta III (DRw52), DR alpha: DR7 beta I, DR alpha: DR4/7 beta IV (DRw53), DQ7 alpha: DQw2 beta, DQ7 alpha: DQw3 beta, and DPw4 alpha: DPw4 beta. These class II-expressing transfectants were used to analyze by flow cytometry the molecular specificities of 20 anti-class II mAb. These analyes indicate that some mAb are more broadly reactive than was previously thought based on immunochemical studies. In contrast, the narrow molecular specificities of other anti-class II mAb were confirmed by this approach. Transfectants expressing human class II molecules should be valuable reagents for studies of B cell and T cell defined epitopes on these molecules.
Development of self-tolerance in normal mice. Appearance of suppressor cells that maintain adult self-tolerance follows the neonatal autoantibody response.
Authors: Miller R D , Calkins C E 
Published: December 2022

Abstract
T cell populations from BALB/c mice at different ages were analyzed to determine when in development Ts cells specific for the anti-mouse RBC (MRBC) autoantibody response become activated. Previous studies have shown that adult CD8+ T cells actively suppress this autoimmune response and adult spleen cells depleted of CD8+ cells can generate an anti-MRBC response in culture with MRBC. The present results demonstrate that T cells from mice less than 1 wk of age do not suppress the in vitro anti-MRBC response of adult spleen cell populations depleted of CD8+ Ts cells. By 2 wk of age Ts cells are detectable in this anti-self response and reach adult levels by 3 wk of age. Non-specific "natural suppressor" cells normally present in neonatal spleen cell populations are unable to suppress this autoantibody response, although they are active in suppressing anti-SRBC responses in the same cultures. Before the appearance of Ts cells active in the anti-MRBC response, neonatal spleen cell populations can generate anti-MRBC antibody-forming cells, both spontaneously in vivo and in vitro. The in vitro anti-MRBC response of neonatal spleen cells was shown to be Ag driven and Ag specific. The ability of unfractionated spleen cells to generate this response in vitro declines with age and is relatively low by 3 wk. This decline in responsiveness occurs simultaneously with the appearance of suppression specific for the anti-MRBC response, suggesting that the two events may be causally related.
Effects of T cell depletion in radiation bone marrow chimeras. I. Evidence for a donor cell population which increases allogeneic chimerism but which lacks the potential to produce GVHD.
Authors: Sykes M , Sheard M , Sachs D H 
Published: December 2022

Abstract
The opposing problems of graft-vs-host disease (GVHD) and failure of alloengraftment present major obstacles to the application of bone marrow transplantation (BMT) across complete MHC barriers. The addition of syngeneic T-cell-depleted (TCD) bone marrow (BM) to untreated fully allogeneic marrow inocula in lethally irradiated mice has been previously shown to provide protection from GVHD. We have used this model to study the effects of allogeneic T cells on levels of chimerism in recipients of mixed marrow inocula. The results indicate that T cells in allogeneic BM inocula eliminate both coadministered recipient-strain and radioresistant host hematopoietic elements to produce complete allogeneic chimerism without clinical GVHD. To determine the role of GVH reactivity in this phenomenon, we performed similar studies in an F1 into parent combination, in which the genetic potential for GVHD is lacking. The presence of T cells in F1 marrow inocula led to predominant repopulation with F1 lymphocytes in such chimeras, even when coadministered with TCD-recipient-strain BM. These results imply that the ability of allogeneic BM cells removed by T cell depletion to increase levels of allochimerism may be mediated by a population which is distinct from that which produces GVHD. These results may have implications for clinical BM transplantation.