bluuebunny/crossref_metadata_2025_split huggingface dataset:
Imbalanced accumulation of ribosomal RNA in macrophages activated in vivo or in vitro to a cytolytic stage.
Authors: Varesio L 
Published: December 2022

Abstract
Previous studies have shown that peritoneal murine macrophages activated in vivo and in vitro to a tumoricidal stage have a depressed rate of RNA synthesis. In attempting to clarify the differences in RNA metabolism between noncytotoxic and tumoricidal macrophages, we have studied the relative accumulation of various species of RNA in macrophages activated in vivo and in vitro with the use of agarose gel electrophoresis. Macrophages activated in vitro to a cytotoxic stage with supernatants containing lymphokines (LK) and traces of lipopolysaccharide (LPS) have an imbalanced accumulation of mature ribosomal RNA (rRNA), with a decreased accumulation of 28S rRNA compared to 18S rRNA. In contrast, macrophages primed in vitro with LK free of detectable endotoxins that exhibit suppressive rather than tumoricidal activity do not manifest a decreased 28S:18S rRNA ratio. The conclusion that the decreased 28S:18S rRNA ratio was associated with the activation of macrophages to a cytolytic stage was supported by the finding that cytotoxic macrophages activated in vivo by i.p. injection of Propionibacterium acnes (formerly designated C. parvum) also demonstrated a decreased accumulation of 28S comparable with that observed in in vitro-activated macrophages. Moreover, activated macrophages that lost their cytolytic activity upon prolonged in vitro culture had an augmented accumulation of 28S rRNA. These results provide the first direct evidence that the expression of cytolytic activity is associated with modulation of a specific class of RNA. The unbalanced accumulation of rRNA appears to be a late molecular event in the activation process occurring during the transition from primed to cytotoxic macrophages, because inflammatory and primed macrophages had normal rRNA accumulation. A model of macrophage activation accounting for these results is proposed.
The antigen receptor on a human T cell line initiates activation by increasing cytoplasmic free calcium.
Authors: Imboden J B , Weiss A , Stobo J D 
Published: December 2022

Abstract
A monoclonal antibody to the antigen-receptor on the T cell line Jurkat induces substantial increases in [Ca++]i. Ca++ ionophores can substitute for this antibody in activation by increasing [Ca++]i to levels comparable with those seen with the antigen-receptor antibody. Stimulation with either the antigen-receptor antibody or a Ca++ ionophore leads to the appearance of the same phosphoproteins. These results suggest that the antigen-receptor initiates T cell activation by increasing [Ca++]i.
Influenza viruses as lymphocyte mitogens. I. B cell mitogenesis by influenza A viruses of the H2 and H6 subtypes is controlled by the I-E/C subregion of the major histocompatibility complex.
Authors: Scalzo A A , Anders E M 
Published: December 2022

Abstract
Influenza A viruses of the H2, H3, and H6 subtypes function as T cell-independent B cell mitogens for lymphocytes from BALB/c mice. Lymphocytes from C57BL/10 mice, however, undergo mitogenesis only in response to H3 viruses. The failure of C57BL/10 lymphocytes to respond to H2 and H6 viruses was shown not to reflect a difference in dose-response profile or kinetics of the response, nor was it due to the activity of suppressor T cells. Experiments with congenic and recombinant strains of mice established that mitogenic responsiveness to H2 and H6 viruses is linked to the major histocompatibility complex, and is controlled by a gene located in the I-E/C subregion. Furthermore, responsiveness was shown to correlate with the expression of surface I-E antigen, being positive for mouse strains that express I-E antigen (haplotypes a, d, k, p, r) and negative for strains that do not (haplotypes b, f, q, s). The data suggest that influenza A viruses of the H2 and H6 subtypes may interact directly with I-E molecules on the surface of B cells or possibly on an accessory cell. Because mitogenesis by H3 viruses is not I-E dependent, it appears that influenza A viruses stimulate B cell mitogenesis by at least two different mechanisms.
Three distinct antigen systems on human B cell subpopulations as defined by monoclonal antibodies.
Authors: Takami T , Ishii Y , Yuasa H , Kikuchi K 
Published: December 2022

Abstract
Three novel antigen systems (L22, L23, and L24) expressed on human B cell subpopulations were identified by using TB1-2C3, TB1-2B3, and TB1-3C1 monoclonal antibodies, respectively. L22 was expressed on a minor subpopulation of B cells in human lymphoid tissues and in the peripheral blood. These B cells associated with L22 were resting small B cells mainly located in the mantle zone of lymphoid follicles, most of which also expressed IgM and IgD on their cell membrane. This antigen was absent from all cultured hemopoietic cell lines including B cell-derived cell lines as well as from all human B cell malignancies, except for B cell-type chronic lymphocytic leukemia and hairy cell leukemia. L23 and L24, on the other hand, existed on approximately two-third of B cells in blood and lymphoid tissues. These L23 and L24 antigens were expressed largely on small lymphocytes located in the mantle zone of lymphoid follicles and to a lesser extent on large blastic cells within lymphoid germinal centers. L23 and L24, like L22, seem to disappear from B cells during their differentiation into antibody-secreting cells, because they were not expressed on normal and neo-plastic plasma cells. This is additionally confirmed by the observation that L23 and L24 were expressed little or not at all on pokeweed mitogen-activated and Epstein-Barr virus-transformed B cells, and were absent from some of B cell malignancies that have been thought to correspond to the later stages of B cell development. Although L23, but not L22 and L24, was faintly expressed on mature granulocytes and monocytes, none of L22, L23, or L24 existed on human thymus and T cells. Immunoprecipitation studies showed that L23 and L24 were different molecular species consisting of a single glycoprotein with m.w. of 205,000 and 145,000, respectively. L22 antigen is presently under study.
Experimental autoimmune myasthenia gravis: can pretreatment with 125I-labeled receptor prevent functional damage at the neuromuscular junction?
Authors: Sterz R K , Biro G , Rajki K , Filipp G , Peper K 
Published: December 2022

Abstract
Rats were immunized with purified receptor from electric fish to induce experimental autoimmune myasthenia gravis (EAMG). It is implied by the clonal selection theory that antigens react only with receptors on specific immunocompetent cell subpopulations. In an attempt to damage these specific cells with the aid of highly radioactive antigen, one group of rats was pretreated with an additional injection of radiolabeled receptor of high specific activity 3 days before the basic immunization. The success of the immunization was monitored by measuring changes in the following three parameters: antibody titers against nicotinic acetylcholine receptor; number of alpha-bungarotoxin-binding sites at endplates; and number of acetylcholine-operated ionic endplate channels, using quantitative electrophysiologic methods. Conventionally immunized animals showed the classical signs of EAMG: elevated antibody titers against nicotinic acetylcholine receptor and a reduction of the number of alpha-bungarotoxin-binding sites, as well as reduction of the number of acetylcholine-operated ionic channels. The same symptoms were found in animals pretreated with unlabeled receptor and in animals pretreated with radioactive albumin. Animals pretreated with radioactively labeled receptor showed far less reduction of functional nicotinic acetylcholine receptor and only slightly raised antibody titers. This study suggests that preimmunization with radioactive antigen selectively eliminates immunocompetent cells, thus precluding the production of antibodies by a subsequent immunization procedure. The same protective effect cannot be obtained by either preimmunization with unlabeled antigen or by radioactively labeled unspecific antigen.
Regulation by interleukin 2 of interleukin 2 receptors and gamma-interferon synthesis by human thymocytes: augmentation of interleukin 2 receptors by interleukin 2.
Authors: Reem G H , Yeh N H 
Published: December 2022

Abstract
The role of interleukin 2 (IL 2) on the expression of IL 2 receptors and on the synthesis of gamma-interferon (gamma-IFN) by human thymocytes was investigated. Human thymocytes isolated from specimens obtained during cardiac surgery of infants and children were induced with one or all of the following agents: IL 2, concanavalin A (Con A), and 12-O-tetradecanoylphorbol 13-acetate (TPA). The expression of IL 2 receptors and gamma-IFN titers were determined. The results indicate that thymocytes cultured in complete medium do not express receptors for IL 2, nor did IL 2 by itself induce the expression of IL 2 receptors. Con A induced the expression of IL 2 receptors by a moderate number of the thymocyte population and induced the synthesis of low amounts of gamma-IFN. Preincubation of thymocytes with TPA increased the response to Con A; both the number of thymocytes expressing receptors and the synthesis of gamma-IFN were increased. Addition of IL 2 to these cultures further augmented the expression of IL 2 receptors and gamma-IFN synthesis and resulted in the optimal expression of IL 2 receptors and maximal gamma-IFN synthesis. The expression of IL 2 receptors could be detected within 24 hr and preceded the induction of proliferation; it was therefore probably not due to the clonal expansion of a population of receptor-bearing thymocytes. Conversely, inhibition of IL 2 synthesis with dexamethasone (Dex) by thymocytes activated with Con A, or inhibition of the function of IL 2 receptors by anti-Tac, resulted in a decrease in the number of IL 2 receptor-bearing thymocytes activated with Con A, or inhibition of the function of IL 2 receptors by anti-Tac, resulted in a decrease in the number of IL 2 receptor-bearing thymocytes and of gamma-IFN synthesis. Thymocytes activated with TPA and Con A were more resistant to the inhibitory effects of Dex on the expression of IL 2 receptors than thymocytes activated with Con A alone. Maximal inhibition of the expression of IL 2 receptors and of gamma-IFN synthesis was achieved as a result of the synergistic effect of anti-Tac with Dex. Therefore, when IL 2 was prevented from binding to the receptors, and IL 2 synthesis was inhibited, the number of thymocytes expressing IL 2 receptors was sharply reduced and gamma-IFN synthesis was markedly inhibited.(ABSTRACT TRUNCATED AT 400 WORDS)
Effect of recombinant IL 2 and gamma-IFN on proliferation and differentiation of human B cells.
Authors: Nakagawa T , Hirano T , Nakagawa N , Yoshizaki K , Kishimoto T 
Published: December 2022

Abstract
The effects of IL 2 and gamma-IFN on the activation of human B cells was studied with recombinant IL 2 and gamma-IFN. BCDF-responsive B lymphoblastoid cell lines and highly purified human B cells were employed as target B cells. IL 2 or gamma-IFN did not induce any IgG or IgM secretion in the B cell lines CESS and SKW6-CL4, in which IgG and IgM were inducible with conventional T cell factor(s). IL 2 alone did not induce the optimum production of Ig, but did induce proliferation in the SAC-stimulated B cell population. No Leu-1-, Leu-4-, or Leu-7-positive cells were detected in B cell populations that had been stimulated with SAC for 3 days. FACS analysis showed that a portion of the SAC-stimulated B cells (30%) were in the G2 or M stages by IL 2 stimulation. The addition of gamma-IFN together with IL 2 induced IgM and IgG secretion in SAC-stimulated B cells that was comparable with that induced by a conventional T cell factor(s). IL 2 induced proliferation not only in SAC-stimulated B cells but also in an anti-mu-stimulated B cell population. Stimulation of T cell populations with anti-mu and IL 2 did not induce significant proliferation, suggesting the direct effect of IL 2 on B cells. Double staining of anti-mu-stimulated B cells with anti-Ig and anti-Tac antibodies demonstrated that anti-mu stimulation induced an increased expression of Tac antigen on surface Ig-positive B cells. All of these results strongly supported the notion that IL 2 was one of the growth factors for B cells, and gamma-IFN was one of the differentiation factors for B cells.
Interleukin 2 enhances the natural killer cell activity of acquired immunodeficiency syndrome patients through a gamma-interferon-independent mechanism.
Authors: Rook A H , Hooks J J , Quinnan G V , Lane H C , Manischewitz J F , Macher A M , Masur H , Fauci A S , Djeu J Y 
Published: December 2022

Abstract
Patients with the acquired immunodeficiency syndrome (AIDS) exhibit a variety of disorders of cellular immunity, including a deficient ability to generate cytotoxic T cells and depressed levels of natural killer (NK) cell activity. Interleukin 2 (IL 2) in vitro can markedly augment these depressed immune functions. Because IL 2 can induce the release of interferon-gamma (IFN-gamma) from normal peripheral blood lymphocytes (PBL), and because IFN-gamma may play a role in the regulation of NK cell activity, this study was performed to determine if the IL 2 enhancement of the NK cell activity of patients with AIDS was an IFN-gamma-dependent effect. PBL from eight healthy heterosexual donors and from nine patients with AIDS were studied for their ability to release IFN-gamma in response to IL 2 at a concentration of 100 U/ml. After 60 hr of culture, the PBL of all eight healthy donors produced IFN-gamma with a mean titer of 113 U/ml (range 40 to 320 U/ml). In contrast, the PBL from only two of nine patients with AIDS released measurable amounts of IFN-gamma (40 U/ml each) in response to IL 2 with a mean titer of 13.5 U/ml for all nine. Although the PBL from patients with AIDS were deficient in their capacity to produce IFN-gamma in response to 100 U/ml of IL 2, significant enhancement of NK cell activity could be obtained after only 1 hr of PBL treatment with 10 U/ml of IL 2, with an optimal NK enhancing effect occurring at doses of 50 to 100 U/ml of IL 2. The use of an anti-IFN-gamma monoclonal antibody resulted in complete neutralization of the IFN released from the normal PBL cultured with IL 2, but failed to inhibit the IL 2 enhancement of NK cell activity. Exogenous IFN-gamma exhibited different kinetics of enhancement of NK cell activity when compared to IL 2, requiring substantially more than 1 hr of pretreatment of PBL. These results indicate that the PBL from patients with AIDS usually do not release IFN-gamma when cultured with IL 2, and that IL 2 enhancement of the depressed NK cell activity of these patients may be an IFN-gamma-independent event. These results may have important implications for the therapy of AIDS.
The isolation and characterization of the human suppressor inducer T cell subset.
Authors: Morimoto C , Letvin N L , Distaso J A , Aldrich W R , Schlossman S F 
Published: December 2022

Abstract
Immunization of mice with lower primate lymphoid cells has provided a useful strategy for raising monoclonal antibodies against functionally important surface determinants on human T lymphocytes. We have developed a monoclonal antibody, anti-2H4, which defines functionally unique human T cell subsets. This anti-2H4 antibody was reactive with approximately 42% of unfractionated T cells, 41% of T4+ inducer cells, and was reactive with approximately 54% of T8+ cytotoxic/suppressor population. Anti-2H4 was not reactive with human thymocytes, but reacted with subsets of peripheral blood B cells and null cells. This antibody subdivided peripheral blood T4+ cells into two functionally distinct populations. The T4+2H4+ subset proliferate well to concanavalin A (Con A) stimulation, but poorly to soluble antigen stimulation, and provides poor help to B cells for PWM-induced Ig synthesis. The T4+2H4- subset, in contrast, proliferates poorly upon stimulation with Con A, but well on exposure to soluble antigen, and provides a good helper signal for PWM-induced Ig synthesis. What is, perhaps, most important, the T4+2H4+ subset functions as the inducer of the T8+ suppressor cells. Previous attempts to define the latter subset of cells has relied heavily on the use of specific autoantibodies present in the sera of patients with juvenile rheumatoid arthritis (JRA) and systemic lupus erythematosus (SLE). The present results suggest that anti-2H4 antibody defines the human suppressor induced subset of lymphocyte previously described as T4+JRA+. Last, the results reemphasize the previously documented remarkable structural conservation of certain T cell-specific determinants on lymphocytes of phylogenetically distant primates.
Failure of bone marrow cells to reconstitute T cell immunity in graft-vs-host mice.
Authors: Lang P , Miller M W , Shearer G M 
Published: December 2022

Abstract
A chronic GVH reaction (detected by T cell immune deficiency) was induced in unirradiated, adult (C57BL/10 X B10.A)F1 mice by injecting them i.v. with 3 X 10(7) B10.A parental spleen cells. Thirty-four days later, attempts were made to reconstitute the GVH immune-deficient mice by whole-body irradiation and repopulation with bone marrow cells from normal syngeneic F1 mice. The reconstituted mice were tested for CTL responses 147 and 272 days after repopulation with normal F1 bone marrow. These GVH/chimera mice remained immunoincompetent for at least 272 days for CTL responses to hapten-self and H-2 allogeneic antigens.
T cell responses to Mls determinants are restricted by cross-reactive MHC determinants.
Authors: Lynch D H , Gress R E , Needleman B W , Rosenberg S A , Hodes R J 
Published: December 2022

Abstract
The studies presented here investigated the relationship between T cell recognition of MHC-encoded products and non-MHC-linked Mls determinants. The first aspect addressed whether Mls-reactive T cells recognize Mls-encoded products alone or in association with MHC-encoded determinants. Initial studies used Mlsa-specific T cell clones that were generated by repeated stimulation of C57BL/6 or B10.A(5R) spleen cells with DBA/2 lymphoid cells. These clones recognized Mlsa on cells expressing MHC products of the H-2b, H-2d, and H-2k haplotypes, but not the H-2q haplotype. Thus, these cloned T cells were found to recognize Mlsa products in association with public but demonstrably polymorphic H-2 determinants. The question of whether T cell clones that were specific for self-H-2 determinants (autoreactive) or soluble antigen plus syngeneic H-2 (antigen-specific) could also be stimulated by Mlsa determinants was also addressed. A substantial proportion of the antigen-specific or autoreactive T cell clones tested were stimulated by Mlsa determinants. Furthermore, stimulation of these clones by Mlsa was H-2 restricted. The pattern of H-2-restricted recognition of Mlsa by these clones was not distinguishable from that observed in the Mlsa-specific T cell clones, nor was it influenced by the primary specificity or H-2 restriction pattern of a given clone. Although these findings provide a means of explaining the observation that Mls-reactive T cells exist at extremely high precursor frequencies, they also raise questions regarding the nature of the receptor structures which are used by a single T cell in the recognition of two or more apparently distinct stimuli.
Frequency analysis of functional immunoglobulin C- and V-gene expression by mitogen-reactive B cells in germfree mice fed chemically defined ultra-filtered "antigen-free" diet.
Authors: Hooijkaas H , van der Linde-Preesman A A , Bitter W M , Benner R , Pleasants J R , Wostmann B S 
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 conventional (CV) and "antigen-free" C3H/HeCr mice of various ages. The antigen-free mice were germfree (GF)-raised and were fed an ultrafiltered solution of chemically defined (CD) low m.w. nutrients, and were thus devoid of exogenous antigenic stimulation. Spleen and BM cells were grown in a limiting dilution culture system that allows the growth and development of every newly formed LPS-reactive B cell into a clone of IgM-secreting cells which are capable of switching to other immunoglobulin (Ig) heavy chain isotypes (C-gene expression). The secretion of IgM and IgG1 was determined in the protein A plaque assay, whereas specific IgM antibody-secreting cells (V-gene expression) were detected in plaque assays specific for various heterologous erythrocytes and sheep red blood cells (SRBC) coupled with a number of different haptens. The absolute frequency of LPS-reactive B cells and their capacity to switch to IgG1-secretion was not significantly different in 8- to 12-wk-old and 52-wk-old GF-CD mice and their age-matched CV controls. Moreover, no differences were observed in the frequencies of antigen-specific B cells within the pool of LPS reactive B cells. These frequencies ranged from 1 in 20 to 1 in 50 for NIP4-SRBC and NNP2-SRBC, from 1 in 100 to 1 in 150 for NIP0.4-SRBC, from 1 in 50 to 1 in 100 for TNP30-SRBC, and from 1 in 1000 to 1 in 2000 for SRBC and horse red blood cells. Within the limitations of having determined the switching capacity of IgM to IgG1 only and having assessed only a minor fraction of the total B cell antibody-specificity repertoire, the data indicate that young and old GF-CD mice, although devoid of exogenous antigenic and/or mitogenic stimulation, generate B cells with a similar switching capacity and a similar IgM antibody specificity repertoire as CV mice.
Coexpression of T4 and T8 on peripheral blood T cells demonstrated by two-color fluorescence flow cytometry.
Authors: Blue M L , Daley J F , Levine H , Schlossman S F 
Published: December 2022

Abstract
Using two-color fluorescence flow cytometry, we were able to detect the presence of small numbers of T4+T8+ cells (about 3%) in freshly isolated peripheral T cell populations derived from normal healthy donors. Coexpression of T4 and T8 was predominantly found on large blastlike cells and appeared to be related to activation. Stimulation of peripheral T cells with concanavalin A (Con A) for 5 days resulted in the generation of up to 60% of T4+T8+ cells. Coexpression was accompanied by a twofold increase in the number of T8 antigenic sites per cell. The T4+T8+ cells in lectin-stimulated cultures expressed high levels of the activation antigens T9, T10, and the IL-2 receptor but lacked T6, an antigen found on a majority of stage II thymocytes. Coexpression of T4 and T8 appeared to be a transitory process, because prolonged culture of T cells in the absence of lectin resulted in the loss of the T4+T8+ phenotype. Our data suggest that T cell activation in peripheral blood results in the generation of a T4+T8+ cell population which is distinct from previously described thymic and peripheral blood cells. Because T4 and T8 molecules may interact directly with MHC antigens, coexpression of these molecules may have an important role in immune function.
Specificity of oligoclonal IgG bands in sera from chronic relapsing experimental allergic encephalomyelitis guinea pigs.
Authors: Mehta P D , Patrick B A , Wisniewski H M 
Published: December 2022

Abstract
The specificity of oligoclonal IgG in sera from chronic relapsing EAE guinea pigs was determined by using imprint electroimmunofixation. The response of oligoclonal IgG to spinal cord and Mycobacterium tuberculosis appeared to be equal in animals sacrificed during first remission and in those sacrificed after recovery from acute EAE. In contrast, in animals sacrificed during or after the first relapse, the oligoclonal IgG seems to be directed predominantly against spinal cord. In imprint electroimmunofixation, the oligoclonal IgG specific to spinal cord did not react with guinea pig liver and kidney. In addition, activity to spinal cord could be removed from sera by absorption with spinal cord but not with kidney or liver.