bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accelerated 86Rb+ (K+) release from the cytotoxic T lymphocyte is a physiologic event associated with delivery of the lethal hit.
Authors: Russell J H , Dobos C B 
Published: December 2022

Abstract
Cloned CTL have been loaded with the K+ analogue 86Rb+. When mixed with unlabeled target cells, accelerated 86Rb+ release occurs from the CTL. The magnitude of accelerated 86Rb+ release is proportional to the efficacy of the target in standard 51Cr release assays. The signal responsible for accelerated 86Rb+ release has been localized to a postbinding event and has the physiologic requirements of delivery of the lethal hit. Thus, accelerated 86Rb+ release from the CTL represents the first direct observation of a physiologic event within the CTL related to a functional CTL-target interaction.
Immunoregulatory human T lymphocytes triggered as a consequence of viral infection: clonal analysis of helper, suppressor inducer and suppressor effector cell populations.
Authors: Meuer S C , Cooper D A , Hodgdon J C , Hussey R E , Morimoto C , Schlossman S F , Reinherz E L 
Published: December 2022

Abstract
The regulatory functions of a series of human T cell clones specific for an autologous Epstein-Barr virus transformed B lymphoblastoid cell line were examined. Two T4+ T cell clones, termed AT4II and AT4IV, and one T8+ clone, AT8III, were maintained in culture for greater than or equal to 9 months and were characterized in detail. Both T4+ clones provided helper function for autologous B cell immunoglobulin production when added to unstimulated peripheral blood mononuclear cells. In addition, these same clones produced soluble inducer factors after specific antigenic stimulation. However, when AT4II, AT4IV and their subclones were tested on pokeweed mitogen stimulated peripheral blood mononuclear cells, it was found that AT4IV provided help for immunoglobulin production whereas AT4II cells were strongly suppressive. This suppression by AT4II was indirect and required the presence of fresh, autologous, unirradiated T8+ cells. In contrast, the T8+ AT8III clone markedly inhibited Ig production by autologous B cells in the absence of any additional T8+ cells from peripheral blood and produced a soluble suppressor factor upon specific antigenic triggering. Thus, after stimulation with autologous Epstein-Barr virus transformed cells, at least three discrete regulatory human T cell populations can be defined at the clonal level: helper, inducer of suppression and suppressor effector clones.
Human lymphocyte function associated antigen-1 (LFA-1): identification of multiple antigenic epitopes and their relationship to CTL-mediated cytotoxicity.
Authors: Ware C F , Sanchez-Madrid F , Krensky A M , Burakoff S J , Strominger J L , Springer T A 
Published: December 2022

Abstract
Human lymphocyte function-associated antigen (LFA)-1, a heterodimeric lymphocyte surface glycoprotein of 177,000 and 95,000 relative molecular weight has been implicated to function in the cytotoxic T lymphocyte (CTL) effector mechanism. Seven mouse hybridoma lines producing monoclonal antibodies (MAb) reactive with this structure were studied. Three unique and 3 partially over-lapping epitopes on human LFA-1 were defined by competitive cross inhibition binding assays using biosynthetically labeled anti-LFA-1 MAb. In contrast, of five rat antimouse LFA-1 MAb, all five recognized a common or shared epitope. An HLA-B7 specific human CTL line expressed 1.1 X 10(5) LFA-1 sites per cell with a direct saturation binding assay. Human CTL expressed two to four times more LFA-1 than peripheral blood lymphocytes or B and T lymphoblastoid cell lines. Titration of each of the anti-LFA-1 MAb in a 51chromium release cytolytic assay revealed quantitative differences in the ability of the different anti-LFA-1 MAb to block cytolysis indicating distinct functional and antigenic epitopes exist on the human LFA-1 molecule. Anti-LFA-1 MAb reversibly inhibited the CTL reaction by slowing the initial rate of cytolysis. These results suggest anti-LFA-1 MAb inhibit CTL function by specific blockade of a functionally relevant molecule.
The use of mutants of Escherichia coli for the identification of human lymphocyte subpopulations in blood smears.
Authors: Bratescu A , Mayer E P , Teodorescu M 
Published: December 2022

Abstract
In previous work we have shown that some bacteria can bind to human lymphocytes and can be used to identify lymphocyte subpopulations in conventionally stained blood smears. These bacteria are of different species or genera, which makes it difficult to study the binding mechanism. Also, the main marker for B cells, Brucella melitensis, is of very small size and highly pathogenic. Here we show that B cells as well as some of the T cell subpopulations can be identified by different mutants obtained from a strain of an Escherichia coli. Two procedures were used to generate mutants. First, E. coli-YS57 (pro-his-trp-) was mutagenized with N-methyl-N'-nitro-N-nitrosoguanidine and the binding to mouse spleen cells was used as a selective pressure. Second, phage-resistant mutants of E. coli-YS57 were obtained and tested for the ability to bind to lymphocytes. Out of 10 strains selected by the former procedure, 5 bound to a significant number of human lymphocytes. All four phage-resistant mutants bound to human lymphocytes. Out of the total of nine mutants that bound to lymphocytes, six bound consistently, i.e., they bound to similar percentages of peripheral blood lymphocytes from different normal donors. One phage-resistant mutant, E. coli USC-106, bound only to B cells. The subpopulations of lymphocytes identified by the mutants were essentially the same as those identified by different species or genera of bacteria. We concluded that E. coli mutants can be obtained that identify human lymphocyte subpopulations and that one of these mutants recognizes B cells; these mutants may be used to study the nature of the receptors for bacteria on lymphocytes, which appear to have a lectin-like nature.
Inhibiton of IL 2 production after human allogeneic bone marrow transplantation.
Authors: Azogui O , Gluckman E , Fradelizi D 
Published: December 2022

Abstract
Bone marrow transplantation (BMT) is currently used to treat patients with severe aplastic anemia or leukemia. Despite the use of an HLA identical sibling donor, however, the survival after BMT is reduced by the occurrence of two major immunologic complications: graft-vs-host disease and a long-lasting immune deficiency responsible for late infections. This immune deficiency could be explained by an imbalance of lymphocyte subpopulations reconstituted after transplant. The aim of the present work was to study the helper function by measuring the production of interleukin 2 (IL 2). This lymphokine is responsible for the amplification of the effector phase of immunity. A consecutive series of 34 patients was tested for IL 2 production after BMT. This production was absent or low in 32 of 34 patients for at least 2 yr after BMT. The mechanism of this low IL 2 production was investigated. Irradiation of patients' lymphocytes in vitro with low dose gamma-rays partially restored the IL 2 production after 6 mo of evolution. The IL 2 production was not restored or was slightly affected by irradiation early after BMT. These results suggest that the lack of immune reconstitution after BMT may be caused by the lack of IL 2-producing cells and/or the increased activity of suppressor cells of the helper function. This suppression is radiosensitive.
Altered expression of lymphocyte Fc alpha receptor in selective IgA deficiency and IgA nephropathy.
Authors: Adachi M , Yodoi J , Masuda T , Takatsuki K , Uchino H 
Published: December 2022

Abstract
To study the expression of FcR specific for IgA (Fc alpha R) on human peripheral lymphocytes (PBL), PBL from normal donors were incubated with 300 to 500 micrograms/ml MOPC 315 IgA having anti-trinitrophenyl (TNP) antibody activity at 4 degrees C or 37 degrees C for 60 min. Under this condition, less than 2% of total cells could form rosettes with TNP-coated ox red blood cells (TNP-ORBC). When cultured with MOPC 315 IgA at 37 degrees C for 18 hr, however, there was a dose-dependent increase of the rosette-forming cells (RFC) binding TNP-ORBC. Because 15 to 20% of the total cells bound TNP-ORBC but not unsensitized ORBC, the rosette formation appeared to be due to the cytophilic binding of IgA to the cells. The binding of MOPC 315 IgA was competed by TEPC 15 IgA and human myeloma IgA, but not by murine myeloma proteins of other classes, indicating that the receptor is specific for IgA. Fc alpha R was induced on 15 to 20% of fractionated T and B cells, as well as on 15 to 18% of concanavalin A-(Con A) activated lymphocytes when cultured with IgA. The induction of the receptor was dependent on protein and RNA synthesis, but not on DNA synthesis as suggested by the sensitivity to metabolic inhibitors, such as mitomycin C, actinomycin D, puromycin, and cycloheximide. In five patients with selective IgA deficiency (serum IgA, 0 to 4 mg/dl), only 5.1% +/- 1.7 of PBL formed rosettes with TNP-ORBC after culture with MOPC 315 IgA, whereas 12.5% +/- 2.5 of PBL from normal donors (serum IgA, 90 to 330 mg/dl) formed rosettes. Fc alpha R was induced on more than 15% of the cells from these patients, however, when cultured with IgA in the presence of a conditioned medium obtained from mixed lymphocyte culture from two normal donors. The results suggested that the abnormality in the patients' PBL might be in the induction mechanism rather than in the number of precursor cells that could express Fc alpha R in the presence of IgA. On the other hand, Fc alpha R was induced on 10.4% +/- 1.5 of PBL from the patients with IgA nephropathy (serum IgA, 382 +/- 11 mg/dl) when they were incubated with IgA for 1 hr at 37 degrees C. Because Fc alpha R on normal PBL was not induced by 1 hr of incubation with IgA, it appeared that the receptor was already expressed in vivo on the cells of these patients.
The effect of the X-linked immune deficiency gene (xid) upon the Y chromosome-related disease of BXSB mice.
Authors: Smith H R , Chused T M , Steinberg A D 
Published: December 2022

Abstract
BXSB mice develop a lupus-like disease characterized by B cell hyperplasia, hypergammaglobulinemia, autoantibodies, nephritis and coronary artery disease. To determine the subset of B cells responsible for disease in these mice, we bred a congenic BXSB.xid strain (greater than 99.2% inbred) with the xid gene that deletes a subset of splenic B cells. Because BXSB disease is associated with the Y chromosome, BXSB males and the autoimmune cross (NZB X BXSB)F1 males were studied. BXSB.xid males had profoundly reduced lymphoid hyperplasia, hypergammaglobulinemia, autoantibodies, renal disease, cardiac disease, and markedly prolonged survival. (NZB.xid/+ X BXSB)F1 males also demonstrated a marked protection associated with the xid gene. These studies suggest that the autoimmune disease of BXSB males is dependent upon the B cell subset deleted by xid.
A rapid biologic assay for the detection of interleukin 1.
Authors: Conlon P J 
Published: December 2022

Abstract
The detection of human peripheral blood-derived IL 1 was accomplished by a modification of the monokine-dependent conversion assay of the cell line LBRM-33 from the IL 2 nonproducer to producer phenotype after incubation with the monokine and lectin. The conversion of the LBRM-33 subclone, 1A5B6, was modified by directly adding the IL 2-dependent cell line CTLL-2 to metabolically inactivated LBRM-33. This enabled the more rapid identification of macrophage-derived IL 1 and was approximately 1000 to 10,000 times more sensitive than the traditional thymocyte proliferation assay. It is hoped that with the assay described here, it will be feasible to more accurately screen for the presence of this important immunoregulatory molecule in an immune response.
Dissociation in expression of MB1/MT1 and DR1 alloantigens in mutants of a lymphoblastoid cell line.
Authors: DeMars R , Chang C C , Marrari M , Duquesnoy R J , Noreen H , Segall M , Bach F H 
Published: December 2022

Abstract
Cytotoxicity tests with alloantisera were used to study the expression of HLA-D region antigens in HLA-DR-null mutants of a human lymphoblastoid cell line. The initial cell line contained just one copy of the MHC as a haplotype that included DR1 and MB1/MT1. Gamma ray mutagenesis of the single haplotype cells followed by selection with complement and an anti-DR monoclonal antibody were then used to isolate DR-null mutants. Two categories of mutants were identified with a panel of alloantisera. Expressions of DR1 and MB1/MT1 were simultaneously lost in four mutants. Nine mutants still expressed MB1/MT1 but had lost the expression of DR1. The dissociated loss of expression of MB1/MT1 and DR1 antigens is evidence for separate genetic control of these alloantigens. The methods used exemplify a versatile approach for conveniently inducing separations of closely linked loci of the MHC.
Enhancement of murine T cell I-J expression by limited proteolysis.
Authors: Klyczek K K , Hullett D A , Hayes C E 
Published: December 2022

Abstract
I-J-encoded structures on peripheral T cells and thymocytes appear normally to be blocked or shielded by material that is susceptible to proteolysis. Limited proteolysis with trypsin, papain, pronase, or chymotrypsin increased the number of peripheral T cells and thymocytes lysed by anti-I-Jk serum and complement. Proteolysis did not induce I-Jk expression on B cells or on negative strain T cells. Increased lysis was enzyme concentration and time dependent and was not due to increased susceptibility of protease-treated cells to lysis by antibody plus complement; proteolysis rendered T cells and thymocytes less susceptible to lysis by anti-H-2Kk, anti-H-2Dd, and anti-Lyt-2 antibodies. Absorption experiments showed that I-Jk determinant density was increased in the protease-treated T cell population. The I-Jk determinants detected are proteins or glycoproteins; extended proteolysis removed these molecules from the T cell surface. Treatment of T cells or thymocytes with activated macrophage culture supernatant containing proteolytic activity produced a small but reproducible increase in I-Jk expression. Proteolysis of lymphocyte membranes, possibly mediated by macrophages, may have a role in cellular differentiation and immune activation.
Alternative pathway of complement activation by human lymphoblastoid B and T cell lines.
Authors: Praz F , Lesavre P 
Published: December 2022

Abstract
Other investigators have reported activation of the alternative complement (C) pathway in homologous and heterologous serum by a variety of human lymphoblastoid B cell lines. Their ability to activate the C was associated with Epstein Barr virus transformation of the cells. We report that some human lymphoblastoid T cell lines, lacking EBV-DNA in their genome, do activate the human alternative C pathway with no participation of immunoglobulin or specific antibodies. Nevertheless, activation measured by C3 deposition on the cell surface was weaker than with the B cell lines so far studied; in relation to the RAJl cells, C3 deposition on JURKAT, MOLT 4, HSB2, and 1301 was, respectively, 68, 38, 28, and 19%. Furthermore, C3 deposition on JURKAT T cell line requires D, whereas RAJl cells provide a proteolytic activity able to mimic D, and which, unlike D, can be controlled by serum protease inhibitors. Although the ability to activate the AP seems to be a largely shared property of the human lymphoblastoid B and T cell lines, the situation was strikingly different with normal and mitogen-stimulated lymphocytes or with acute leukemic cells, which led to a negligible AP-dependent C3 deposition compared with the level observed with the lymphoblastoid cell lines. Membrane sialic acid content was determined for every cell tested and revealed no relationship with their ability to activate the AP. The two EBV+ B cell lines tested led to a comparable AP activation regardless of the presence of the C3b receptor.
Ocular herpes simplex virus infection is diminished by depletion of B lymphocytes.
Authors: Jordan C , Baron S , Dianzani F , Barber J , Stanton G J 
Published: December 2022

Abstract
Rabbit anti-mouse mu-chain serum was used to deplete specifically IgM-bearing B cells and B cell function in BALB/c mice. B cell-depleted and normal littermates were infected via the cornea with herpes simplex virus type 1 (HSV-1) at 4 to 5 wk of age. B cell-depleted mice had a reduced number of lymphocytes bearing surface immunoglobulin and a greatly reduced ability to produce antibody. Mortality was reduced from 89% in normal controls to 42% in B cell-depleted mice (p less than 0.001) and peak virus shedding from eyes was also reduced as much as 90% in the B cell-depleted mice (p less than or equal to 0.0005). These results support the hypothesis that a B cell function of normal mice somehow contributes directly or indirectly to the enhanced mortality of mice infected with HSV.
Biochemical analysis of a 130,000 molecular weight glycoprotein on human melanoma cells.
Authors: Albino A P , Lloyd K O , Ikeda H , Old L J 
Published: December 2022

Abstract
A monomeric sialoglycoprotein of 130,000 molecular weight (gp 130) is a membrane protein detected by mouse monoclonal antibodies on human melanoma cells and in lesser amounts on a wide range of normal and malignant cell types. Eight monoclonal antibodies reacting with gp 130 detect at least four spatially distinct epitopes on the exposed surface of the gp 130 molecule. Biosynthetic studies have shown that gp 130 is synthesized through two precursor forms: a 100 kD glycosylated species and an 80 kD unglycosylated species, presumably the primary translational product of the encoding mRNA.
Frequency analysis of functional immunoglobulin C and V gene expression in murine B cells at various ages.
Authors: Hooijkaas H , Preesman A A , Van Oudenaren A , Benner R , Haaijman J J 
Published: December 2022

Abstract
The frequencies of lipopolysaccharide- (LPS) reactive B cells and their antibody specificity repertoire have been determined in the spleen and bone marrow (BM) of mice at different ages. A limiting dilution culture system was employed that allows the growth and development of every LPS-reactive B cell into a clone an IgM-secreting cells that are capable of switching to other Ig heavy chain isotypes (C gene expression). The secretion of IgM and IgG1 was assessed in the protein A plaque assay, whereas specific IgM antibody-secreting cells (V gene expression) were detected with the use of plaque assays specific for various heterologous erythrocytes and sheep red blood cells (SRBC) coupled with a number of different haptens. The frequencies of LPS-reactive B cells in the spleen and BM of C3H/Tif, C57BL/Ka, BALB/c, and CBA/Rij mice appeared to be similar in 6- to 12- and 100-wk-old animals, as was the switch frequency to IgG1 secretion in three strains tested. Moreover, no age-related changes were observed in the frequencies of antigen-specific B cells within the pool of LPS-reactive B cells in the spleen and BM of C57BL/Ka mice. The frequencies ranged from 1 in 10 to 1 in 20 for NIP4- and NNP2-SRBC, from 1 in 50 to 1 in 100 for TNP30-SRBC, and from 1 in 1000 to 1 in 4000 for SRBC, HRBC, and GRBC. The specificity repertoire of the "spontaneously" occurring ("background") IgM-secreting cells in the spleen and BM, on the other hand, did differ between young and old C57BL/Ka mice. During aging the frequencies of the tested specificities decreased in the spleen but increased in the BM. Our data indicate that in unintentionally immunized mice the clonal selection of B lineage cells by antigen takes place at the level of the mature, antigen-reactive B cell.
Epstein-Barr virus induces normal B cell responses but defective suppressor T cell responses in patients with systemic lupus erythematosus.
Authors: Tsokos G C , Magrath I T , Balow J E 
Published: December 2022

Abstract
Epstein-Barr virus (EBV) is a polyclonal B cell activator, independent of helper T cells, which induces the generation of suppressor T cells in vivo and in vitro. Given the complexity of the immunologic abnormalities in patients with systemic lupus erythematosus (SLE), we used EBV as a tool to examine the following questions: a). Are SLE B cells primarily defective? and b). Does EBV stimulate the generation of suppressor activity from SLE T cells? It was found that B cells from SLE patients infected with EBV in vitro generate plaque-forming cell (PFC) responses that are similar to those raised by normal B cells infected with EBV within the first 14 days of culture. T cells from SLE patients, in contrast to T cells from normal individuals, cultured with autologous B cells plus EBV fail to develop the expected normal decrement of PFC during the late phase of the in vitro culture (day 14). However, B cells from SLE patients are susceptible to suppression as mixed cultures of SLE B cells and normal allogeneic T cells showed a pattern of PFC response to EBV similar to that of the co-culture of normal B cells with normal T cells. T cells from SLE patients, in analogous mixed cell cultures, failed to suppress either normal B cells or allogeneic SLE B cells. The above experiments indicate that the B cells are not intrinsically defective in SLE patients; rather, a specific T cell abnormality contributes to the lack of normal immunoregulation of certain B cell responses in SLE.
Release of platelet activating factor in rabbits with antibody-mediated injury of the lung: the role of leukocytes and of pulmonary endothelial cells.
Authors: Camussi G , Pawlowski I , Bussolino F , Caldwell P R , Brentjens J , Andres G 
Published: December 2022

Abstract
This paper describes the release of platelet-activating factor (PAF) into the circulation of rabbits with acute pulmonary injury induced by antibody reacting with pulmonary endothelium. Eight rabbits were injected i.v. with 2 mg/kg of body weight of goat anti-rabbit lung angiotensin-converting enzyme gamma-globulin (GtARbACE). All animals developed acute pneumonitis, characterized by severe endothelial damage, accumulation of polymorphonuclear leukocytes (PMN) and platelets (Plt) in the lumina of alveolar capillaries, and deposits of goat IgG and rabbit C3 along alveolar capillary walls. Six of the rabbits died from acute pulmonary edema. PAF was detected in the plasma of all animals within 5 min after injection of GtARbACE. Five other rabbits were depleted of leukocytes by nitrogen mustard and then injected with 2 mg/kg of body weight of GtARbACE. In three of these rabbits release of PAF was demonstrated, though in amounts smaller than in non-leukocyte-depleted rabbits; all three animals died from pulmonary edema. After injection of 0.03 mg/kg of body weight of GtARbACE in six additional rabbits, three of them leukocyte-depleted, small amounts of PAF were detected in the circulation. None of these six rabbits died of pulmonary edema. PAF release was not observed in ten rabbits injected i.v. with 2 or 0.03 mg/kg of body weight of normal goat gamma-globulin. In separate experiments in vitro, incubation of isolated lung or thoracic aorta with GtARbACE resulted in deposits of goat IgG along endothelia and significant release of PAF. PAF was also released from endothelial cells removed from thoracic aorta by cellulose acetate paper and then incubated with GtARbACE. When segments of thoracic aorta were stripped of endothelium and then incubated with GtARbACE, PAF release could not be shown. The data obtained are consistent with the interpretation that PAF released into the circulation after binding of GtARbACE to the endothelia of lung and aorta originates from leukocytes and from lung and thoracic aorta endothelial cells.