bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cell cycle analysis of lymphocyte activation in normal and autoimmune strains of mice.
Authors: Raveche E S , Steinberg A D , DeFranco A L , Tjio J H 
Published: December 2022

Abstract
The spontaneous spleen cell proliferation and the proliferation induced by in vivo or in vitro stimulation with such polyclonal B cell activators (PBA) as LPS, poly rI.rC, and anti-mu were studied in normal and autoimmune mice. The various murine models of autoimmunity differ in the level of naturally occurring splenic cellular hyperactivity as well as in the ability of their spleen cells to be further stimulated in vitro by polyclonal stimulators. Both the NZB strain and the MRL/Ipr strain had markedly increased numbers and percentages of spontaneously proliferating spleen cells, whereas the BXSB strain did not. Nonautoimmune strains were found to have very small numbers of activated cells in the spleen. However, such normal strains could be induced in vivo to mimic the natural splenic hyperactivity observed in older NZB and MRL/Ipr autoimmune strains by the injection of polyclonal B lymphocyte stimulators. In contrast, old hyperactive NZB mice were not further induced to undergo proliferation by in vivo administration of such stimulators. Density-separated, T depleted, spleen cells of normal and autoimmune mice were stimulated in vitro with PBA in 48-hr cultures. Cells from old MRL/Ipr and NZB mice were abnormal in both the anti-mu response and the LPS response; BXSB mice had normal anti-mu responses. These studies suggest that there is no prerequisite for spontaneous splenic hyperactivity in the development of autoimmunity. In addition, different PBA stimulate separate subsets of B cells that differ in their state of activation in the various autoimmune strains. Finally, different B cell subsets appear to be abnormal in different types of autoimmune mice.
Long-term in vitro culture of murine mast cells. III. Discrimination of mast cells growth factor and granulocyte-CSF.
Authors: Yung Y P , Moore M A 
Published: December 2022

Abstract
Long-term in vitro growth of murine mast cells was dependent on the presence of a mast cell growth factor (MCGF) present in media conditioned by mitogen-activated splenic leukocytes or by various murine leukemic cell lines. MCGF shared a number of properties with granulocyte colony-stimulating factor (G-CSF). Both factors were present in media conditioned by the myelomonocytic leukemic WEHI-3 and the T cell lymphoma, LBRM-33 cell lines. They were relatively sensitive to trypsin treatment, and were resistant to boiling temperature. NZB mice that failed to respond to WEHI-3-derived G-CSF also failed to respond to MCGF. MCGF differed from G-CSF, however, in sensitivity to neuraminidase and lactoferrin, an inhibitor of macrophage CSF production, suppressed G-CSF production by WEHI-3 cells without affecting MCGF production. Furthermore, peritoneal cells produced G-CSF but not MCGF when stimulated with lipopolysaccharide. In vitro production of MCGF by normal spleen cells required the presence of T lymphocytes and is relatively macrophage-independent. The role of T cells in the maturation and growth of mast cells and the physiologic function of MCGF are discussed.
Dissociation between cutaneous basophil hypersensitivity and basophil sensitization.
Authors: Lett-Brown M A , Thueson D O , Grant J A 
Published: December 2022

Abstract
We investigated the antigen-specific sensitization of basophils in the peripheral circulation of guinea pigs using an in vitro histamine release assay. Animals were primed for cutaneous basophil hypersensitivity (CBH) by intradermal injection of either keyhole limpet hemocyanin (KLH) or ovalbumin (OA) in saline. Basophils isolated from these animals 7 days after sensitization did not release histamine to the specific antigen in vitro. On day 9, however, basophils did release histamine when challenged with the antigen. These results were in contrast to 24-hr skin tests that showed a typical CBH profile both on day 7 and day 9. When animals were immunized via the footpad by emulsification of antigen in incomplete Freund's adjuvant, basophil sensitization (i.e., histamine release) either occurred earlier (day 7, KLH) or at lower antigen concentrations (OA). Thus, dissociation of in vivo CBH and in vitro basophil sensitization was demonstrated. The lack of correlation was only seen early after immunization and depended on the route of immunization used. An additional finding was a transient blood basophilia that also was dependent on the route of immunization, the antigen used, and the time post-sensitization. Our results are consistent with the hypothesis that at early times post-immunization, CBH is mediated by T cells and not via homocytotropic antibodies, but that at later times such antibodies may also play a role in the elicitation of CBH reactions.
Altered levels of mononuclear leukocytes in tumor-bearing rats: decrease of helper T lymphocytes and increase of suppressor cells.
Authors: Fernandez-Cruz E , Gilman S C , Feldman J D 
Published: December 2022

Abstract
In the spleen and peripheral blood of BN rats with progressive tumors, W3/25+ T helper cells were significantly reduced and OX8+ T suppressor/cytotoxic cells were significantly increased. The ratio of helper to suppressor elements was decreased to 1.6 from a ratio of 3 in normal BN rats without tumors, and this decreased ratio correlated with tumor growth. When tumors were eliminated in vivo by infusion of effector cells (W3/25+ T lymphocytes), the levels of W3/25+ and OX8+ T cells returned to normal and the ratio of helper to suppressor/cytotoxic cells in the spleen and peripheral blood reverted to 3.0 or higher. Macrophages and null cells, T-sIg-, were also elevated in the spleen and peripheral blood of rats bearing expanding tumors and returned to normal levels after cure. Assays of spleen cells for cell-mediated cytotoxicity in rats with large tumors revealed little or no specific cytotoxicity. Cytotoxic activity was high in spleen of rats cured of their neoplasms by infusion of helper cells.
Inhibition of cytotoxic T lymphocyte activity by concanavalin A.
Authors: Sitkovsky M V , Pasternack M S , Eisen H N 
Published: December 2022

Abstract
Several lectins were tested for the ability to interfere with the recognition or lysis of target cells by cytotoxic T lymphocytes (CTL). Of those tested, concanavalin A (Con A) had the greatest effect: at 0.25 to 10 micrograms/ml, it profoundly blocked antigen-specific lysis of target cells by cloned and uncloned CTL in various allo- and syngeneic systems. Separate pretreatment of CTL and target cells showed that the effect of Con A is exercised predominantly on CTL. Various experimental results ruled out several possible explanations for the inhibitory effect of Con A, such as: CTL-CTL self-killing by nonspecific, lectin-dependent cytotoxicity, impairment of lateral mobility of CTL surface components, and cell agglutination, preventing recycling of CTL among target cells. The findings suggest that subagglutinating concentrations of Con A block CTL activity by binding to and interfering with CTL surface structures that have relatively high affinity for Con A and are critically involved in recognition or lysis of target cells.
Formation of IgE-binding factors by rat T lymphocytes. VI. Cellular mechanisms for the formation of IgE-potentiating factor and IgE-suppressive factor by antigenic stimulation of antigen-primed spleen cells.
Authors: Uede T , Ishizaka K 
Published: December 2022

Abstract
Analysis of cellular mechanisms of formation of IgE-binding factors by KLH-primed spleen cells revealed that the presentation of KLH to KLH-primed T cells by adherent cells resulted in the formation of lymphokines that in turn stimulated unprimed lymphocytes to form IgE-binding factors. Lymphokines released from KLH-alum-primed spleen cells induced normal lymphocytes to form IgE-potentiating factors, whereas those released from KLH-CFA-primed spleen cells induced the formation of IgE-suppressive factors. Fractionation of the lymphokines from KLH-primed spleen cells and analysis of cell sources of the lymphokines revealed that multiple factors are involved in the selective formation of one or the other IgE-binding factors. Thus, KLH-alum primed splenic T cells from "inducers" of IgE-binding factors and glycosylation-enhancing factors upon antigenic stimulation, and these factors in combination stimulate unprimed W 3/25+ Fc gamma R+ T cells to form IgE-potentiating factors. Antigenic stimulation of KLH-CFA-primed T cells results in the formation of the "inducers" and glycosylation-inhibiting factors, and these two lymphokines collectively stimulate unprimed W 3/25+ Fc gamma R+ T cells to form IgE-suppressive factors. Cell sources of "inducers" are W 3/25+ Fc gamma R- T cells, cells different from the source of IgE-binding factors. The glycosylation-enhancing factor is derived from W 3/25+ F gamma R+ T cells in KLH-alum-primed spleen; the glycosylation-inhibiting factor is derived from OX 8+ T cells in KLH-CFA-primed spleen. Evidence was obtained that these lymphokines, which modulate the protein glycosylation of IgE-binding factors during their biosynthesis, are derived from antigen-primed T cells and determine the nature of IgE-binding factors formed.
Abnormalities of immunoregulatory T cell subsets in patients with insulin-dependent diabetes mellitus.
Authors: Horita M , Suzuki H , Onodera T , Ginsberg-Fellner F , Fauci A S , Notkins A L 
Published: December 2022

Abstract
Patients with insulin-dependent diabetes mellitus (IDDM) have autoantibodies that react with cells in the islets of Langerhans. To determine whether these patients suffer from a more generalized immunoregulatory disorder, the ratio of phenotypic helper to suppressor cells was evaluated by specific monoclonal antibodies. Our experiments showed that the helper/suppressor cell ratio was significantly increased in patients with IDDM of less of 2 mo duration and then gradually returned to normal. Despite the alteration in the helper/suppressor cell ratio, there was no evidence for polyclonal activation as measured by the number of immunoglobulin-secreting plaque-forming cells in the peripheral blood. There was, however, a significant increase in the number of spontaneous plaque-forming cells in patients suffering from both IDDM and Hashimoto's thyroiditis (HT). Nonetheless, immunoglobulin production after stimulation with pokeweed mitogen was not different in diabetics with or without HT when compared to normal controls. These findings suggest that subtle changes in the immunoregulatory system occur during the early stages of IDDM.
A monoclonal antibody against a surface antigen shared by human large granular lymphocytes and granulocytes.
Authors: Rumpold H , Kraft D , Obexer G , Böck G , Gebhart W 
Published: December 2022

Abstract
A monoclonal IgM antibody VEP13 was raised against a cell membrane antigen by immunizing BALB/c mice with a cell preparation enriched for human large granular lymphocytes (LGL). These cells are known to include the effector cells responsible for natural killer (NK) and killer (K) cell activity. By indirect immunofluorescence, VEP13 antibody reacted with 21.4 +/- 7.9% of peripheral blood lymphocytes (PBL) and more than 95% granulocytes but not with B lymphocytes, monocytes, erythrocytes, thrombocytes, thymocytes, and immature bone marrow cells. Cell suspensions enriched for T cells by means of E-rosetting using neuraminidase-treated sheep red blood cells contained 14.7 +/- 5.5% of VEP13+ cells. When PBL were treated with VEP13 antibody and complement, NK activity against a variety of target cells was greatly reduced and K cell activity was also strongly affected. Enrichment experiments of VEP13+ cells by means of the fluorescence-activated cell sorter revealed that all the NK activity resides in the VEP13+ fraction. This cell fraction was a homogeneous population of LGL. Studying the coexpression of various other antigens as defined by monoclonal antibodies, 84.6 +/- 4.6% of VEP13+ cells also expressed M1, 81.6 +/- 5.5% T10, 47.9 +/- 14.4% Leu 2a, 51.6 +/- 17.0% human Lyt-3, and 6.0 +/- 4.0% HLA-DR antigens. Leu 1, Leu 3a, and T6 antigens were found to be absent from VEP13+ cells. We conclude that VEP13 antibody should be helpful in determining LGL in peripheral blood as well as in tissue sections of tumor patients.
In vitro influenza virus-specific antibody production in man: antigen-specific and HLA-restricted induction of helper activity mediated by cloned human T lymphocytes.
Authors: Lamb J R , Woody J N , Hartzman R J , Eckels D D 
Published: December 2022

Abstract
Cloned human T lymphocytes induced with influenza A virus (A/Texas/1/77) and maintained in continuous culture with T cell growth factor were assayed for helper function in the in vitro production of anti-influenza antibody. Helper function mediated by both cloned helper T cells and normal peripheral blood lymphocytes was highly antigen dose-dependent, requiring lower concentrations than that necessary to induce blastogenesis. Optimal help was observed with 1 X 10(2) cloned T cells per culture, whereas excess helper cells inhibited the response. After culture with influenza A virus-induced cloned helper T cells, the antibodies formed were directed against influenza A and not B virus. Furthermore, the cloned helper T cells despite being specific for matrix protein collaborated in the production of predominantly anti-hemagglutinin antibody, suggesting associative recognition of the two discrete antigens. Cellular interactions between cloned helper cells from an HLA-Dw1,3 DR1,3 individual and erythrocyte rosette-negative cells required HLA-Dw1; DR1 compatibility for the production of specific antibody. This was confirmed by using subclones. Finally, it was observed that supernatants of the cloned helper T cells contained functional activity capable of replacing the parent cells in the production of anti-influenza A virus antibody.
Two subgroups of HLA Bw44 defined by cell-mediated lympholysis that differ in Bw44 expression on platelets and in patterns of genetic linkage disequilibrium.
Authors: Tekolf W A , Biddison W E , Aster R D , Shaw S 
Published: December 2022

Abstract
Possible immunogenic heterogeneity of the HLA-Bw44 antigen was investigated using cytotoxic T lymphocytes (CTL) generated between donors identical for HLA-A2,3,-B7,w44. Highly discriminatory CTL combinations were identified that defined two subgroups of Bw44, designated 44.1 and 44.2. Out of 47 Bw44-positive donors tested in a population study, 30 were lysed by the CTL defining 44.1, and 19 were lysed by the CTL defining 44.2. All Bw44 cells could be typed as either 44.1 or 44.2, except two Bw44-positive cells that were phenotypically homozygous for the serologically defined Bw44 antigen and were lysed by both CTL. No Bw44-negative donors (zero out of 37) expressed either 44.1 or 44.2, although cold target blocking was required to eliminate a contaminating reactivity of one CTL population on Bw35 and some Bw45 cells. CTL were also raised between responder/stimulator combinations mismatched for Bw44. These CTL lysed all Bw44-positive target cells, indicating a CML antigen shared by all Bw44 cells. But clear discrimination of the 44.1 and 44.2 subgroups was obtained when appropriate cold target blocking cells were added. All donors with 44.2 expressed high levels of serologically detectable Bw44 on their platelets, and all with 44.1 expressed low levels (p less than 0.005). Furthermore, population studies indicate that 44.1 is in positive linkage disequilibrium with HLA-A2 and possibly DR4, whereas 44.2 is in positive linkage disequilibrium with HLA-DR7 and possibly HLA-A23, -A26, and -A29. These data suggest the existence of two genetically and functionally different subgroups of Bw44 antigens.
The murine sex-limited protein (Slp): reassessment of its sex limitation.
Authors: Ferreira A , Eichinger D , Nussenzweig V 
Published: December 2022

Abstract
Previous studies in which an alloantiserum was used to measure Slp levels indicated that in certain inbred strains of mice (Slpa), this protein was sex-limited, that is, present only in males. We raised several monoclonal antibodies directed against different epitopes of Slp and used them to develop a sensitive two-site immunoradiometric assay. Using this assay we detected Slp in serum of all Slpa females previously thought to be phenotypically negative. The levels of Slp in these females are about 0.2 to 4% of that of the males of the same inbred strain. The molecule found in serum of females was isolated by affinity chromatography and was found to have the characteristic three-chain structure of male Slp. These findings establish that the presence of Slp in Slpa females is the rule rather than the exception. Quantitative differences similar in magnitude to those found between males and females were also detected among Slpa males; i.e., Sd males have about 100 times more Slp than Sp males. The mechanisms by which androgens determine the extensive quantitative male-female differences, and by which the S region determines large variations among Slpa males, are unknown.
Three M components IgA lambda, + IgG kappa n + IgG kappa h in one patient. II. Structurally different kappa n and kappa h chains associated with H(gamma) chains sharing idiotypic determinants.
Authors: Bouvet J P , Liacopoulos P , Pillot J , Banda R , Tung E , Wang A C 
Published: December 2022

Abstract
Structural analysis of purified IgG kappa h and IgG kappa n molecules of DA myeloma paraproteins indicated that the two IgG had different electrophoretic mobility and that L-kappa h had an unusually heavy m.w. (30,000). Peptide mapping showed the existence of additional peptides in the L-kappa h map when compared to the L-kappa n map. Total amino acid analysis showed that L-kappa h contained two additional cysteine residues and certain other amino acids than L-kappa n contained. Sequence of the first 25 NH2-terminal amino acids showed differences at positions 4, 5, 15, 18, and 21, but both L-kappa h and L-kappa n belong to the same V kappa IV subgroup. IgG kappa n but not IgG kappa h reacted with anti-gamma 1 antiserum, indicating that H chains of these two paraproteins were also different. Sera from rabbits immunized with IgG kappa n or IgG kappa h, and rendered specific for idiotypic determinants by appropriate absorption, were used for idiotype characterization of these components. Immunodiffusion, immunoelectrophoresis, and direct hemagglutination demonstrated that IgG kappa h and IgG kappa n cross-reacted partially. Inhibition tests disclosed that the main anti-idiotypic antibody was directed against a conformation structure of the complete IgG kappa h molecule, whereas cross-reaction was due to partial idiotypic similarity between H chains of the IgG kappa h and IgG kappa n. In addition, each of these paraproteins seemed also to bear private idiotypes on their H and L chains.
Immune responses to complex protein antigens I. MHC control of immune responses to bovine albumin.
Authors: Riley R L , Wilson L D , Germain R N , Benjamin D C 
Published: December 2022

Abstract
Murine T cell proliferative and antibody responses to the multi-determinant protein bovine serum albumin (BSA) are controlled by Ir genes mapping within the H-2 gene complex. Strains possessing the H-2k, H-2a, and H-2d haplotypes are classified as high responders to BSA. In contrast, H-2b strains are low responders to BSA. Genetic mapping experiments employing strains with recombinant H-2 haplotypes indicate that both T cell proliferative and antibody responses are at least in part regulated by genes within the I-A subregion. Studies on the inhibition of T cell proliferation by monoclonal anti-Ia antibodies are consistent with the assignment of an Ir gene for BSA to the I-A subregion and strongly suggest a role for genes within the I-E/C subregions as well. The MHC-mediated control of antibody responses did not affect the affinity or the isotype of the antibody produced. The relative quantities of antibody specific for each of the three domains of BSA appears to be regulated by H-2-linked BSA Ir genes, and domain III antigenic determinants were found to be dominant in the responses of low-responder mice and in the early response of high-responder mice. This domain III epitope dominance essentially disappears by the tertiary response of high-responder mice.
Inhibition of basophil histamine release by anti-inflammatory steroids. II. Studies on the mechanism of action.
Authors: Schleimer R P , MacGlashan D W , Gillespie E , Lichtenstein L M 
Published: December 2022

Abstract
The glucocorticosteroids inhibit the IgE-dependent release of histamine by human basophils with an order of potency that very closely parallels that found in vivo (i.e., triamcinolone acetonide greater than dexamethasone greater than beta-methasone greater than prednisolone greater than hydrocortisone much greater than progesterone approximately tetrahydrocortisone approximately 0). The effect is seen after a 24-hr preincubation with nanomolar to micromolar concentrations of glucocorticoid. In contrast, release of histamine stimulated by the formyl methionine containing peptide f-met-leu-phe, the calcium ionophore A23187, and the tumor-promoting phorbol diester 12-O-tetradecanoylphorbol-13-acetate was not inhibited by 24-hr incubation with the potent glucocorticoid dexamethasone. Dexamethasone inhibited anti-IgE-induced histamine release without altering its rate, suggesting that the glucocorticoids do not inhibit histamine release by elevating the intracellular level of cAMP. Dexamethasone did not consistently alter either the total or occupied basophil IgE Fc receptor number, and therefore the glucocorticoid effect does not appear to be due to the modulation of cell surface Fc epsilon receptor content. These data indicate that steroid hormones inhibit basophil IgE-dependent activation through a specific glucocorticoid receptor. The mechanism by which they do so appears not to involve an elevation of cAMP or a shedding of cell surface Fc epsilon receptors. Further, because the glucocorticoids did not inhibit release initiated by the PLA2-dependent stimuli f-met-leu-phe, A23187 and TPA, the inactivation of IgE-dependent histamine release by glucocorticoids may not be the result of PLA2 inhibition.