bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibodies to the common leukocyte antigen (T200) inhibit an early phase in the activation of resting human B cells.
Authors: Mittler R S , Greenfield R S , Schacter B Z , Richard N F , Hoffmann M K 
Published: December 2022

Abstract
T191, a monoclonal antibody reactive with the T200 common leukocyte antigen, profoundly inhibits an early event(s) associated with alpha-immunoglobulin M (alpha IgM)/T cell replacing factor (TRF) or alpha IgM/recombinant interleukin 1 and 2 (rIL 1 and rIL 2)-induced tonsillar B cell proliferation. Kinetic analysis of T191-mediated inhibition indicated that the antibody exerts its effect within 12 to 24 hr of the initiation of cultures and rapidly loses its activity thereafter. Small resting B cells are most sensitive to T191 inhibition, whereas B cells with increasing buoyant density (presumably reflecting stages of increased activation) become progressively T191 insensitive. Analysis of RNA synthesis subsequent to alpha IgM crosslinking of surface immunoglobulin demonstrated that T191 reduced [3H]uridine incorporation by up to 38% during the first 20 hr of culture. In contrast to the effects seen with alpha IgM stimulated B cells, T191 had no inhibitory effect upon phorbol myristate acetate-induced B cell proliferation. The inhibitory effect upon B cell proliferation observed with T191 is not unique among other alpha-T200 antibodies. Four of five previously described alpha-T200 monoclonal antibodies had similar inhibitory effects (82 to 57% maximum inhibition of [3H]thymidine incorporation). However, 13.3, an alpha-T200 monoclonal antibody previously shown to block natural killer (NK) cell-mediated killing was without effect. Likewise, those antibodies capable of inhibiting B cell proliferation failed to block NK-mediated cytolysis. Antibody binding experiments together with proliferation inhibition studies suggest that all of the monoclonal antibodies tested recognized distinct epitopes on the T200 antigen. Both observations are of significance because they demonstrate that the effects seen with anti-T200 antibodies represent an interference with highly specific functional regions on the T200 molecules.
Fetal intestinal transplants in syngeneic rats: a developmental model of intestinal immunity.
Authors: Kantak A G , Goldblum R M , Schwartz M Z , Rajaraman S , Ladoulis C T , Goldman A S 
Published: December 2022

Abstract
We conducted a longitudinal study of the development of lymphoid tissue in fetal small intestine transplanted to a subcutaneous site in adult syngeneic Fischer strain rats. Fetal jejunoileal segments obtained between 18 and 21 days of gestation were transplanted to a dorsal subcutaneous site on syngeneic adult rats. Three weeks later, intestinal segments greater than 2.5 cm in length were found in 70% of recipients. Each week for 6 wk post-transplantation, a full-thickness biopsy was obtained for histologic and immunohistologic examination. At the time of transplantation, fetal rat intestine did not display Peyer's patches, intraepithelial lymphocytes, lymphoid follicles, or IgA-containing plasma cells. These lymphoid structures reached adult levels by 4 wk after transplantation, and the sequence of development of the lymphoid structures in the transplants appeared to match the postnatal development of normal small intestine. After immunizing the in situ intestine or the transplanted fetal intestine with cholera toxin, the number of cells producing specific antibodies to the immunogen increased significantly in intestinal transplants and in situ intestine. In contrast, few if any cells synthesizing antibodies to cholera toxin developed in the transplants after i.p. immunization. This study suggests that fetal intestinal transplants behave as part of the mucosal immune system. This model may provide useful approaches to studying the development of mucosal immunity.
Susceptibility of astrocytes to class I MHC antigen-specific cytotoxicity.
Authors: Skias D D , Kim D K , Reder A T , Antel J P , Lancki D W , Fitch F W 
Published: December 2022

Abstract
Cell-mediated immune mechanisms contribute to tissue injury within the central nervous system (CNS) in a number of experimental diseases, including experimental allergic encephalomyelitis and some viral infections, and may mediate lesion formation in multiple sclerosis. We investigated the conditions under which murine astrocytes can become susceptible targets of cytotoxic T cells. We demonstrate that mouse astrocytes in vitro can be susceptible targets of class I major histocompatibility complex (MHC)-specific cytotoxicity mediated by L3 cytotoxic T lymphocytes (CTL). Expression of appropriate class I MHC antigen on the astrocytes is a requirement, because only cells bearing the H-2d phenotype are susceptible to lysis by L3 cells. BALB/c-H-2dm2 astrocytes lacking the specific determinant recognized by L3 cells are not susceptible to lysis. Astrocyte lysis can, however, occur under culture conditions in which MHC antigen expression is immunocytochemically low or undetectable. Cytolysis can be inhibited by pretreatment of the effector L3 cells with either anti-Lyt-2 monoclonal antibody (mAb) or anti-clonotypic mAb and by preincubation of the glial target cells with an appropriate anti-H-2 antibody (anti-H-2Ld). mAb to lymphocyte function-associated antigen does not inhibit cytotoxicity of the L3 clone against glial cells. Knowledge regarding the role of CTL within the CNS, including the surface molecules involved in glial cell lysis, could further the development of immunotherapies designed to effect immune reactivity within the CNS.
IL 1-like activities present in murine amniotic fluid. A significantly larger amount of IL 1 beta-like activity is present in the amniotic fluid of autoimmune NZB mice.
Authors: Jyonouchi H , Voss R M , Good R A 
Published: December 2022

Abstract
Rapid progress in studies of cytokines have clarified their roles in processes of lymphocyte proliferation and differentiation. However, the involvement of these molecules in lymphopoiesis during embryonic development has not yet been well documented. In this study we screened for possible existence of cytokines that influence lymphopoiesis in murine amniotic fluid (AF) obtained from non-autoimmune prone "normal" strains of mice (CBA/J, BALB/c, A/J, SWR, and C57B/6) and autoimmune-prone NZB mice. Significant colony stimulating activity-1 (CSA-1)-like activities were found in AF of all of the strains tested, but relatively low activities were present in AF of NZB mice. No interleukin 2 (IL 2) or interleukin 3 (IL 3)-like activities were detected, Weak IL 1-like activity was found in AF of most of the strains tested; however, the results of the standard thymocyte proliferation assays varied with each AF sample. This variation is probably related to the presence of nonspecific inhibitors including alpha-fetoprotein in murine AF. Therefore, pooled AF from CBA and NZB strains of mice were subjected to several purification procedures to assess the actual amount of IL 1-like activity present in murine AF. After (NH4)2SO4 precipitation and hydrophobic phenyl-Sepharose chromatography, the measurable level of IL 1-like activity could be increased significantly. With lentil-lectin affinity chromatography, IL 1-like activity was completely dissociated from CSA-like activity. Moreover, a significantly larger amount of IL 1-like activity was found in NZB AF fractions (approximately sixfold higher). Apparent pI values estimated by preparative isoelectric focusing (IEF) were 5.9, 7.2, and 7.4 in CBA AF fractions, and 6.5 and 7.3 in NZB AF fractions. The NZB AF fraction with pI of 7.3 showed significantly higher IL 1 activity than the other fractions studied. These partially purified molecules were found to be resistant to pH 2 and the reducing agent, 2-mercaptoethanol, but were inactivated by heat (56 degrees C, 1 hr) or trypsin. None of the fractions showed IL 2-like activity but some that had IL 1-like activity induced IL 2 production in a IL 1-dependent, IL 2-producing B lymphoma cell line. Apparent m.w. of these IL 1-like activities were 14,000, 14,500, 17,000, 18,000, and 21,000 in CBA AF fractions, and 15,000, 19,000, and 21,000 in NZB AF fractions according to SDS-polyacrylamide gel electrophoresis.(ABSTRACT TRUNCATED AT 400 WORDS)
Role of the interleukin 2 receptor in differentiation of a clone of Ly-1+ B cells.
Authors: Bishop G A , Haughton G 
Published: December 2022

Abstract
CH12.LX, an in vitro subclone of a murine B cell lymphoma that makes IgM reactive with sheep erythrocytes (SRBC), has cell surface receptors for the lymphokine interleukin 2 (IL 2). The binding of recombinant murine IL 2 to these receptors did not stimulate CH12.LX cells to differentiate and secrete antibody. However, the binding of either of two monoclonal antibodies (Mab) specific for the IL 2 receptor increased the proportion of CH12.LX cells that secrete hemolytic IgM. The effect did not require the presence of antigen. One of the Mab, 3C7, is known to block the binding of IL2 to its receptor on T cells, whereas the other, 7D4, which also reacts with the IL 2 receptor, does not block the binding of IL 2. The differentiation of CH12.LX induced by 3C7, but not that induced by 7D4, was inhibited by recombinant IL 2. Neither IL 2 (up to 200 U/ml) nor 3C7 (up to 10 micrograms/ml) had any significant influence on incorporation of [3H]thymidine; 7D4 at 10 micrograms/ml decreased thymidine incorporation by about 60%. Mitomycin C and hydroxyurea, which both inhibit the incorporation of [3H]thymidine into CH12.LX cells, also both induce antibody secretion. In both cases, the concentration necessary to cause differentiation is substantially lower than that needed to cause detectable inhibition of thymidine uptake. We conclude that the IL 2 receptor on CH12.LX cells is a functional signal transducing molecule, and we discuss the possible inverse relationship between proliferation and differentiation.
Regulation of the alternative pathway of complement by pH.
Authors: Fishelson Z , Horstmann R D , Müller-Eberhard H J 
Published: December 2022

Abstract
Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia. The abnormal PNH erythrocytes are highly susceptible to complement-mediated lysis in vitro, especially at pH 6.4. Lysis has been shown to be due to alternative pathway activation. The purpose of this study was to determine why lysis of PNH erythrocytes is increased at acidic pH. The results presented demonstrate that at pH 6.4: binding of C5 and Factor B to C3b deposited on human erythrocytes is markedly enhanced; generation of the two C3 convertases, C3(H2O), Bb and C3b,Bb is increased; and control of C3b on human erythrocytes by CR1 and Factor I is diminished. In addition, it was found that rabbit erythrocytes, which activate the human alternative pathway, are also lysed much better at pH 6.4 than at pH 7.4. These results indicate that the optimal pH for the initiation and amplification of the alternative complement pathway, and probably also for the activation of the membrane attack complex, is 6.4.
Phorbol myristate acetate and the calcium ionophore A23187 synergistically induce release of LTB4 by human neutrophils: involvement of protein kinase C activation in regulation of the 5-lipoxygenase pathway.
Authors: Liles W C , Meier K E , Henderson W R 
Published: December 2022

Abstract
Phorbol myristate acetate (PMA), a tumor-promoting phorbol ester, and the calcium ionophore A23187 synergistically induced the noncytotoxic release of leukotriene B4 (LTB4) and other 5-lipoxygenase products of arachidonic acid metabolism from human neutrophils. Whereas neutrophils incubated with either A23187 (0.4 microM) or PMA (1.6 microM) alone failed to release any 5-lipoxygenase arachidonate products, neutrophils incubated with both stimuli together for 5 min at 37 degrees C released LTB4 as well as 20-COOH-LTB4, 20-OH-LTB4, 5-(S),12-(R)-6-trans-LTB4, 5-(S),12-(S)-6-trans-LTB4, and 5-hydroxyeicosatetraenoic acid, as determined by high pressure liquid chromatography. This synergistic response exhibited concentration dependence on both PMA and A23187. PMA induced 5-lipoxygenase product release at a concentration causing a half-maximal effect of approximately 5 nM in the presence of A23187 (0.4 microM). Competition binding experiments showed that PMA inhibited the specific binding of [3H]phorbol dibutyrate ([3H]PDBu) to intact neutrophils with a 50% inhibitory concentration (IC50) of approximately 8 nM. 1-oleoyl-2-acetyl-glycerol (OAG) also acted synergistically with A23187 to induce the release of 5-lipoxygenase products. 4 alpha-phorbol didecanoate (PDD), an inactive phorbol ester, did not affect the amount of lipoxygenase products released in response to A23187 or compete for specific [3H]PDBu binding. PMA and A23187 acted synergistically to increase arachidonate release from neutrophils prelabeled with [3H]arachidonic acid but did not affect the release of the cyclooxygenase product prostaglandin E2. Both PMA and OAG, but not PDD, induced the redistribution of protein kinase C activity from the cytosol to the membrane fraction of neutrophils, a characteristic of protein kinase C activation. Thus, activation of protein kinase C may play a physiologic role in releasing free arachidonate substrate from membrane phospholipids and/or in modulating 5-lipoxygenase activity in stimulated human neutrophils.
Induction of an anti-hepatitis B surface antigen response in mice by noninternal image (Ab2 alpha) anti-idiotypic antibodies.
Authors: Schick M R , Dreesman G R , Kennedy R C 
Published: December 2022

Abstract
Anti-idiotype antibodies to a mouse monoclonal antibody A-12 directed against HBsAg were produced in rabbits. The anti-Id consisted of an Ab-2 alpha preparation that did not display any detectable internal image activity. Immunization of BALB/c mice with the anti-Id (Ab-2 alpha) coupled to KLH induced an anti-HBs response without subsequent HBsAg exposure. No anti-HBs was detected in control groups of mice immunized with other rabbit anti-Id-KLH preparations. The anti-HBs containing sera from mice immunized with the Ab-2 alpha were able to inhibit the Id-anti-Id reaction, indicating that an Id-positive, anti-HBs response was induced. This idiotype is not normally expressed during the murine immune response to HBsAg and suggests that noninternal image anti-Id activates silent clones. This study, along with our previous results obtained with the use of internal image anti-Id, suggests that there is more than one Id network operational during the BALB/c murine immune response to HBsAg.
The mechanisms of antiviral immunity induced by a vaccinia virus recombinant expressing herpes simplex virus type 1 glycoprotein D: clearance of local infection.
Authors: Martin S , Rouse B T 
Published: December 2022

Abstract
We have shown that immunization of mice with a vaccinia virus recombinant expressing glycoprotein D of Herpes simplex virus (HSV)-1 will induce a variety of L3T4+ T cell responses. These included a HSV-specific delayed-type hypersensitivity response, T cell help for the induction of antiviral antibodies, and the ability to eliminate a challenge dose of HSV from the pinna. This protection against a subcutaneous virus challenge was not mediated by the delayed-type hypersensitivity response because intravenous inoculation of the vaccinia virus recombinant expressing HSV-1-gD induced a state of split tolerance. Thus, mice could still clear a HSV challenge inoculum from the pinna yet were unable to mount a HSV-specific delayed-type hypersensitivity response. Evidence is presented that suggests the protective response was, at least, in part mediated by a T cell-dependent induction of virus-neutralizing antibodies. Evidence is also presented that may suggest the failure of a vaccinia virus recombinant expressing HSV-1-gD to induce HSV-specific cytotoxic T cell responses appears to minimize the protective response to only efficiently clearing low 10(4) 50% tissue culture infective dose) challenge populations of virus. These findings are discussed with relevance to the immune control of HSV infections and to the future development of anti-HSV vaccines.
The diversity of the secondary Salmonella typhimurium-specific B cell repertoire.
Authors: Metcalf E S , Gaffney M , Duran L W 
Published: December 2022

Abstract
This report describes the first analysis of the expressed B cell repertoire specific for a bacterium. In this study, responses to an acetone-killed and dried preparation of Salmonella typhimurium strain TML (AKD-TML) are described. The results show that AKD-TML can stimulate splenic B cells from primed CBA/Ca mice over a wide dose range. The average frequency of secondary TML-specific B cells is 16.4 per 10(5) splenic B cells. This frequency is similar to that observed for another complex, natural antigen, the hemagglutinin of influenza virus. The majority of all secondary TML-specific B cells (greater than 70%) secrete immunoglobulin M, but most of these clones also secrete other isotypes of which immunoglobulins G2 and A are the most prevalent. Analysis of the specificity of secondary TML-specific B cells showed that the vast majority of these B cells were specific for the lipopolysaccharide (LPS) molecule. Moreover, fine specificity analysis demonstrated that approximately two-thirds of these anti-LPS-specific B cell clones are directed against the core polysaccharides or lipid A regions of the LPS molecule, while only about one-third are directed toward the O antigen region. Since anti-S. typhimurium serum antibodies are directed primarily against the O antigens, these studies suggest that the serum levels of antibodies to a given epitope on a bacterial antigen may not be a true reflection of the expressed B cell repertoire when analyzed at the single B cell level. These studies also suggest that the role of antibodies to lipid A molecules in the development of protective immunity to S. typhimurium be reevaluated.
Development and regulation of chlamydia-responsive murine B lymphocytes.
Authors: Levitt D , Danen R 
Published: December 2022

Abstract
We have examined characteristics of chlamydia-stimulated mouse B cells as well as cells that regulate polyclonal responses in vitro. B lymphocyte proliferation stimulated by chlamydia arises at a similar time as Escherichia coli lipopolysaccharide (LPS)-induced proliferative responses during ontogeny. In contrast, development of immunoglobulin (Ig)-secreting cells after chlamydia stimulation is delayed by several weeks relative to ontogeny of LPS-inducible plaque-forming cells (PFC). The lack of Ig secretion by immature B cells is not due to a deficiency of Lyb5+ B lymphocytes, since X-linked immunodeficient (xid) NBF1 mice that lack this B lymphocyte population respond well to chlamydia stimulation. Adherent cells are important for chlamydia-stimulated B lymphocyte differentiation, but are not as necessary for their proliferation. Neither adult adherent cells nor T cells can correct the inability of immature spleen cells to develop into Ig-secreting cells; spleen cells from 2-wk-old mice (i.e., immature B cells) will not suppress adult B lymphocyte responses to chlamydia. When B lymphocytes are separated according to their buoyant densities, chlamydia stimulates low density (activated) B cells to proliferate and differentiate better than high density (resting) cells. Proliferative responses to chlamydia arise earlier during ontogeny, do not require adherent cells, and can proceed to a relatively greater extent in resting B cell population (compared with activated B cells) than induction of Ig-secreting cells.
Role of c-myc and other genes in interleukin 2 regulated CT6 T lymphocytes and their malignant variants.
Authors: Cleveland J L , Rapp U R , Farrar W L 
Published: December 2022

Abstract
The cloned murine cytotoxic T cell line CT6 solely requires interleukin 2 (IL 2) for viability and cell cycle progression. Treatment of G arrested cultures of CT6 cells with recombinant IL 2 induces the rapid sequential expression of the nuclear proto-oncogenes c-fos, c-myc, and c-myb but does not affect the expression of several cytosolic or membrane-associated proto-oncogenes. A comparison of early genes induced by growth factor treatment of quiescent NIH/3T3 fibroblasts and CT6 cells demonstrated that only c-fos and c-myc induction is shared in the two different lineages. Factor-independent lines derived from CT6 cells show no mitogenic response to IL 2, yet binding of IL 2 with its receptor in the cells was capable of inducing the expression of c-fos and c-myc. In factor-independent cell lines, c-myc was uniformly expressed at high constitutive levels, suggesting that c-myc abrogates growth factor requirements of these cells. The levels of c-myc expression in the factor-independent lines was not due to an autocrine production of IL 2 but may be a consequence of constitutively activated IL 2 receptors.
Reaction of T lymphocytes with anti-T3 induces translocation of C-kinase activity to the membrane and specific substrate phosphorylation.
Authors: Nel A E , Bouic P , Lattanze G R , Stevenson H C , Miller P , Dirienzo W , Stefanini G F , Galbraith R M 
Published: December 2022

Abstract
Reaction of the T cell membrane with monoclonal antibodies to T3 can initiate cellular activation, and this is associated with increased intracellular Ca2+ and inositol-trisphosphate (IP3) release. We therefore studied the possible involvement of Ca2+/phospholipid-dependent kinase (C-kinase) in these phenomena. Quantitative assays of exogenous substrate phosphorylation in unstimulated cells showed Ca2+/phospholipid-dependent kinase activity in the cytosol, but no comparable activity in the particulate fractions corresponding to membrane and cytoskeleton material. At concentrations of soluble anti-T3 that partially activate T cells in the absence of macrophages, there was a 50 to 60% decrease in C-kinase activity in the cytosol, with a comparable increase in activity in the membrane fraction. A similar transfer of activity was also induced with the known C-kinase activator, 12-O-tetradecanoyl-phorbol-13-acetate, although redistribution was more rapid in onset, more complete, and more sustained. Redistribution of enzyme activity was additionally confirmed by qualitative assays of endogenous substrate phosphorylation. Labeling of intact cells followed by immunoprecipitation analysis with anti-T3 indicated signal-dependent phosphorylation of two components of the T3 complex and an unidentified 94,000 substrate that was resistant to reduction and alkylation. These findings are consistent with an important role for C-kinase in transduction of membrane events by the T3-Ti complex.