bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rejection of fetal neocortical neural transplants by H-2 incompatible mice.
Authors: Nicholas M K , Antel J P , Stefansson K , Arnason B G 
Published: December 2022

Abstract
In order to examine questions concerning immunologic privilege of the central nervous system, we placed neocortical transplants into cerebral ventricles of mice. We compared the fates of transplants between fully H-2 compatible (isografts) and H-2 incompatible (allografts) animals. Histologic evaluation comparing animals from iso- and allograft groups revealed significant differences in the number of inflammatory cells and in the degree of necrosis within the grafts. Response to allografted tissue within the brain mimics that seen in several immune-mediated diseases of the nervous system in that neurons appear to be selectively spared. Only upon subsequent stimulation of the host's immune system with an orthotopic skin graft bearing the major histocompatibility complex antigens of the neural graft are neurons destroyed. Immunohistochemical evaluation revealed that the inflammatory cell infiltrates in and around the allografts were composed of Lyt-2+, L3T4+, and Mac-1+ cells. In addition, Ia+ endothelial cells as well as Ia+ parenchymal CNS cells were found in both donor and host tissue of allografted animals. Hence, H-2 incompatible neural tissue transplanted to the CNS is recognized and rejected by the immune system of the recipient animal. The cellular infiltrates seen within the first weeks to months following transplantation of allogeneic CNS tissue resemble those seen in other allografts undergoing rejection. We conclude that the CNS is not unconditionally privileged as either a transplant site or as a source of transplanted tissue.
Effect of B cell stimulatory factor-1 (interleukin 4) on Fc epsilon and Fc gamma receptor expression on murine B lymphocytes and B cell lines.
Authors: Conrad D H , Waldschmidt T J , Lee W T , Rao M , Keegan A D , Noelle R J , Lynch R G , Kehry M R 
Published: December 2022

Abstract
Culture of murine splenic B cells with interleukin 4 (IL-4) caused the up-regulation of the lymphocyte Fc receptor for immunoglobulin E (IgE) (Fc epsilon R) over a similar dose range as required for Ia up-regulation. However, the expression level of the Fc receptor for immunoglobulin G (Fc gamma R) did not increase, rather IL-4 caused a slight but consistent decrease in the Fc gamma R level on the B cells. Fc epsilon R+ B hybridoma cells also responded to IL-4 by exhibiting increased Fc epsilon R expression; with the hybridoma cells Fc gamma R levels were unaffected. IL-4 caused an increase in the number of Fc epsilon R per cell and the highest levels of expression were obtained by having both IgE and IL-4 present in the culture. The specificity of the increase was demonstrated by blocking IL-4-mediated actions with monoclonal anti-IL-4 (11B11). Experiments following the incorporation of [35S]methionine into the Fc epsilon R demonstrated that IL-4 increased the rate of Fc epsilon R biosynthesis; this provides an explanation for the IL-4-induced increase in Fc epsilon R expression. IL-4, unlike IgE, had no effect on the rate of degradation of the Fc epsilon R. Interferon-gamma (IFN-gamma) totally abrogated IL-4-mediated Fc epsilon R up-regulation; at the same concentration of IFN-gamma Ia up-regulation is also suppressed, although not as effectively. IFN-gamma was shown to directly suppress Fc epsilon R synthesis, thereby explaining the inhibitory action on Fc epsilon R levels. Finally, it was shown that 11B11 inhibited the increased expression of Fc epsilon R on B cells obtained from mice during the early, but not the late, stages of Nippostrongylus brasiliensis infection. This latter finding suggests that the high Fc epsilon R levels seen early in parasite infections are dependent upon IL-4. The results overall provide further insight into the biologic activities of IL-4.
Identification of variants of the basophilic leukemia (RBL-2H3) cells that have defective phosphoinositide responses to antigen and stimulants of guanosine 5'-triphosphate-regulatory proteins.
Authors: Woldemussie E , Ali H , Takaishi T , Siraganian R P , Beaven M A 
Published: December 2022

Abstract
Antigen immunoglobulin E-mediated secretion of histamine from RBL-2H3 cells is associated with substantial hydrolysis of membrane inositol phospholipids and a rise in the concentration of cytosol Ca2+ (calcium signal). Such responses differed among cloned variant lines of the RBL-2H3 cell line from undetectable (1A3 bromodeoxyuridine-resistant (BUDRR), 2B1 BUDRR, and 1B3 BUDRR lines) to about 80% of those in the parent RBL-2H3 cells. In all but one line (1B3 thioguanine-resistant (TgR)), the intensities of the phosphoinositide response and of the calcium signal were correlated with the secretory response. The 1B3 TgR line had no detectable calcium signal (as measured by quin 2 fluorescence or uptake of 45Ca2+) but paradoxically showed modest rates of hydrolysis of inositol phospholipids and of secretion. The responses of the 1B3 TgR line were, however, dependent on the presence of external Ca2+ ions. The induction of secretion with antigen, therefore, was invariably associated with the hydrolysis of inositol phospholipids, but it was not necessarily associated with a change in concentration of cytosol Ca2+. All antigen unresponsive clones could secrete when synergistic signals were induced by exposure to the Ca2+ -ionophore, A23187 and the phorbol ester, 12-O-tetradecanoylphorbol 13-acetate. These lines, otherwise, had immunoglobulin E receptors and had no obvious defect in their capacity to synthesize the inositol phospholipids or in their phenotypic expression of phospholipase C as measured in cell extracts. One finding of possible relevance to the role of guanosine 5'-triphosphate-regulatory proteins in the activation of phospholipase C was the inability of one antigen-nonresponsive line to respond to NaF (in intact cells) or to guanosine 5'-(3-O-thio)triphosphate (in electrically permeabilized cells).
Glucocorticoids suppress calcium mobilization and phospholipid hydrolysis in anti-Ig antibody-stimulated B cells.
Authors: Dennis G , June C H , Mizuguchi J , Ohara J , Witherspoon K , Finkelman F D , McMillan V , Mond J J 
Published: December 2022

Abstract
Glucocorticoids have been shown to play a major role in influencing the activation of B lymphocytes. In view of our recent observation that dexamethasone exerts a marked suppressive effect on an early event in B cell activation that is stimulated by anti-Ig antibody, we investigated its activity on other stimuli that induce intracellular events similar to those produced by anti-Ig antibody. Because the intracellular events that occur after B cell stimulation with phorbol myristate acetate and the calcium ionophore A23187 appear to mimic those that occur after B cell stimulation with anti-Ig antibody, we studied whether the cellular responses elicited by these activation stimuli are affected in a similar fashion by dexamethasone. Whereas anti-Ig antibody-stimulated entry of G0 B cells to the G1 and S phase of the cell cycle was markedly suppressed by dexamethasone, phorbol myristate acetate/A23187 stimulation of these events was resistant to dexamethasone. Our finding that anti-Ig-induced cross-linking of B cell surface Ig, as measured by surface Ig capping, was not inhibited by dexamethasone suggested that corticosteroids inhibit anti-Ig-induced B cell proliferation at a step distal to membrane Ig cross-linking and proximal to phosphatidylinositol bisphosphate hydrolysis. This hypothesis is supported by experiments presented in this manuscript which demonstrate that dexamethasone inhibits anti-Ig-stimulated phosphatidylinositol bisphosphate hydrolysis. We also found that dexamethasone markedly inhibited anti-Ig antibody-stimulated increases in intracellular ionized calcium concentrations. This dexamethasone-mediated suppression is time-dependent as it is not seen when B cells are cultured with dexamethasone for less than 6 hr. Our data suggest that the immunomodulatory activity of glucocorticoids is exerted by binding to its nuclear receptor, thereby preventing the generation of second messengers required for cell activation after agonist-receptor interaction.
Regulation of murine IgE production in SJA/9 and nude mice. Potentiation of IgE production by recombinant interleukin 4.
Authors: Azuma M , Hirano T , Miyajima H , Watanabe N , Yagita H , Enomoto S , Furusawa S , Ovary Z , Kinashi T , Honjo T 
Published: December 2022

Abstract
Serum IgE levels were determined in different strains of mice with enzyme-linked immunosorbent assay by using rat monoclonal anti-murine IgE antibodies in normal and in Nippostrongylus brasiliensis-infected mice. After infection, serum IgE levels were high in BALB/c and CB-20, low in SJL/J and SJA/20 mice, and not detected at all in SJA/9 and nude mice. Surface IgE-positive cells were greatly increased in BALB/c and SJL/J mice after infection, but not in SJA/9 and nude mice. Most surface IgE-positive spleen cells were also surface IgM- and surface IgD-positive. When spleen cells from SJA/9 or nude mice were stimulated in vitro with lipopolysaccharide and recombinant interleukin 4 (formerly B cell-stimulating factor 1), IgE was produced and detected in the supernatants of these cultures. In addition, surface IgE-positive cells could be detected in these cultures. Most of the surface IgE-positive cells were surface IgM- and surface IgD-negative, unlike those seen in the spleens of Nippostrongylus-infected BALB/c and SJL/J mice. These observations show that SJA/9 and nude mice have IgE-producing precursor B cells, and after appropriate stimulation interleukin 4 can induce them to secrete IgE.
Antigen presentation by hapten-specific B lymphocytes. V. Requirements for activation of antigen-presenting B cells.
Authors: Liano D , Abbas A K 
Published: December 2022

Abstract
Splenic B cells specific for the haptens, 2,4,6-trinitrophenyl (TNP) or fluorescein isothiocyanate (FITC) were cultured with a range of concentrations of unmodified or TNP- or FITC-conjugated conalbumin and the conalbumin + I-Ak-specific, interleukin (IL) 1-dependent helper T cell clone, D10 . G4, in the presence and absence of IL-1. Lymphokine secretion, T cell proliferation, and antibody secretion by B cells all exhibited identical antigen dose responses. Thus, hapten-binding B cells presented low concentrations of haptenated conalbumin for activation of both the T and the antigen-presenting B cells. Whereas proliferation of D10 . G4 required the addition of IL-1, both lymphokine production and stimulation of B cells to antibody secretion occurred without exogenous IL-1. These results demonstrate that when B lymphocytes function as presenting cells for antigens that bind to their immunoglobulin receptors, activation of the responding T cells and the B cells themselves occur at similar concentrations of antigen. Moreover, for functional T-B interactions, antigen-presenting B and responding T lymphocytes constitute a complete system that requires no other accessory stimuli, whereas clonal expansion of T cells is dependent on accessory factors such as IL-1. Finally, since D10 . G4 secretes IL-4 but neither IL-2 nor interferon-gamma, our results demonstrate that differentiation of B cells as a consequence of direct ("cognate") interactions with helper T cells as well as of bystander B cells can occur in the absence of IL-1, IL-2, and interferon-gamma.
Production of cytotoxic factor for oligodendrocytes by stimulated astrocytes.
Authors: Robbins D S , Shirazi Y , Drysdale B E , Lieberman A , Shin H S , Shin M L 
Published: December 2022

Abstract
Stimulation of rat astrocytes in vitro by calcium ionophore A23187 and/or lipopolysaccharide results in the generation of a cytotoxic factor that is functionally similar to the previously described macrophage-derived cytotoxic factor, tumor necrosis factor. Like the macrophage product, the astrocyte cytotoxic factor kills murine L 929 cell targets. In addition, it kills rat oligodendrocytes, the myelin-producing cells of the central nervous system. Human recombinant tumor necrosis factor also has cytotoxic activity directed against rat oligodendrocytes.
Activation of plasma Hageman factor and kallikrein in ongoing allergic reactions in the skin.
Authors: Atkins P C , Miragliotta G , Talbot S F , Zweiman B , Kaplan A P 
Published: December 2022

Abstract
Ten atopic subjects, sensitive to intradermal injection of less than or equal to 10 protein nitrogen units of ragweed or grass pollen antigen, underwent paired antigen and buffer skin chamber incubation over the base of denuded skin blisters. The chamber fluids were sampled over a 6-hr period for histamine and activated Hageman factor and plasma kallikrein which were complexed to C1 inhibitor. In 9 of 10 subjects significantly (p less than 0.01) increased histamine levels (74 +/- 11 ng/ml vs 1.5 +/- 0.55 ng/ml) and kallikrein-C1 inhibitor complexes (2.15 +/- 0.78 ng/ml/hr vs 0.51 +/- 0.09 ng/ml/hr, p less than 0.25) were detected at antigen sites compared with buffer sites, respectively. Increased levels of activated Hageman factor (ng/ml/hr) were detected at antigen sites (1.35 +/- 0.60) compared with buffer sites (0.11 +/- 0.05), (p less than 0.01), in 8 of 10 subjects. Whereas peak levels of histamine were obtained after 1 hr of challenge, both Hageman factor and kallikrein activation, as assessed by complex formation, tended to peak later from the 2nd to the 5th hr. This represents the first demonstration that cutaneous IgE-mediated allergic responses are associated with local activation of the intrinsic plasma coagulation-kinin pathways.
Monoclonal antibody characterization of Plasmodium falciparum antigens in immune complexes formed when schizonts rupture in the presence of immune serum.
Authors: Chulay J D , Lyon J A , Haynes J D , Meierovics A I , Atkinson C T , Aikawa M 
Published: December 2022

Abstract
When Plasmodium falciparum parasites are cultured with some immune sera, merozoites are agglutinated by antibodies to form immune clusters of merozoites and prevent their invasion into erythrocytes. Within these immune clusters of merozoites, several antigens that are normally found in the soluble fraction after detergent extraction accumulate in relatively insoluble immune complexes. From mice immunized with these immune complexes, we obtained hybridomas secreting monoclonal antibodies (mAb) that react with various immune clusters of merozoites antigens, including mAb 3D5, which recognizes a 101-kDa antigen (p101) and mAb, 5E3, which recognizes a 113-kDa antigen (p113). Both mAb reacted with antigens at the surface of schizonts, in the vacuolar space, and at the surface of merozoites before their release from schizont-infected cells. Both p101 and p113 were synthesized by mature trophozoites and young schizonts. In pulse-chase experiments, p113 was processed to 100-, 70-, 55-, and 50-kDa products. Both p101 and p113 appeared in the culture medium when schizont rupture occurred in normal culture medium but were found in immune complexes when schizont rupture occurred in the presence of immune serum. Antibodies in immune complexes, when dissociated with acid and used to probe immunoblots, reacted with affinity-purified p101 and p113. Antigens such as these, which are accessible at the parasite surface and react with antibodies present in immune serum that inhibits parasite invasion, are logical candidates to study in the search for a vaccine against the erythrocytic stages of malaria.
IgG antibody subclasses in human filariasis. Differential subclass recognition of parasite antigens correlates with different clinical manifestations of infection.
Authors: Hussain R , Grögl M , Ottesen E A 
Published: December 2022

Abstract
The four subclasses of IgG are distinct in structure, function, and degree of participation in the antibody response to complex antigens. Looking for differential responsiveness of potential pathogenetic significance, we have analyzed both quantitatively and qualitatively the filaria-specific IgG subclass responses of 20 patients with lymphatic filariasis presenting either with chronic lymphatic obstructive pathology and elephantiasis (CP) or with asymptomatic microfilaremia (MF). Subclass-specific monoclonal antibodies were used in an enzyme-linked immunosorbent assay to study IgG filarial antibodies quantitatively and in immunoblot analyses to determine qualitatively the subclass antibody specificities. Quantitatively, the most significant differences among patient groups were in levels of IgG4, which were more than 17 times higher in MF patients (geometric mean, 64.7 micrograms/ml) than in those with CP (mean, 3.7 micrograms/ml). When qualitative analyses were done on the same sera, major differences were noted, particularly in the recognition profiles of the IgG1, IgG3, and IgG4 responses. IgG1 and IgG3 responses to antigens were seen especially to antigens with m.w. greater than 68,000 in all patients with elephantiasis, whereas MF patients showed most of their reactivity to antigens less than 68,000. For IgG4, the MF patients showed prominent recognition of antigens throughout the entire range of m.w., whereas those with CP had very little IgG4 recognition of antigens of any m.w. Interestingly, this relationship was essentially reversed in the IgG3 antibody responses (especially to antigens greater than 68,000) and, to a lesser extent, the IgG1 responses. These findings demonstrate correlations of potential cause/effect significance between IgG4 antibody responsiveness and the immunomodulated asymptomatic MF form of clinical filariasis and between IgG3/IgG1 antibody responsiveness and the clinical presentation of CP.
Regulation by anti-CD2 monoclonal antibody of the activation of a human T cell clone induced by anti-CD3 or anti-T cell receptor antibodies.
Authors: Yssel H , Aubry J P , de Waal Malefijt R , de Vries J E , Spits H 
Published: December 2022

Abstract
In this study the effect of anti-cluster designation (CD) 2 monoclonal antibodies (mAb) on the activation of a cloned human T cell line, HY837, after triggering the CD3/T cell receptor (TcR) complex by anti-CD3 or anti-TcR mAb is described. HY837, which reacts with a series of mAb directed at different epitopes on the TcR, could be induced to proliferation and interleukin 2 (IL-2) production by soluble mAb directed at the CD3/TcR complex in the absence of accessory cells. mAb directed at the CD2 epitope T11-1 were shown to block the IL-2 production by HY837, as well as the expression of the IL-2 receptor, induced by anti-CD3 mAb, resulting in the inhibition of the proliferative response. The effect of anti-CD2 mAb on the proliferative response of HY837, induced by anti-CD3 mAb, was not due to a competition for Fc binding sites. In contrast, the proliferative responses and IL-2 production of HY837, induced by mAb directed at the TcR, were shown to be enhanced by the action of the anti-CD2 mAb. These results indicate that effects mediated by anti-CD3/TcR mAb cannot always be extrapolated to antigen-mediated effects and show that anti-CD2 mAb may regulate the T cell response, induced by mAb directed at the CD3/TcR complex, depending on which part of this complex is triggered during activation.
Immune response to human immunodeficiency virus. In vivo administration of anti-idiotype induces an anti-gp160 response specific for a synthetic peptide.
Authors: Zhou E M , Chanh T C , Dreesman G R , Kanda P , Kennedy R C 
Published: December 2022

Abstract
Anti-idiotypic antibodies (anti-Id) to chimpanzee antibodies directed against a synthetic peptide corresponding to a native epitope associated with gp41 of human immunodeficiency virus (HIV) envelope glycoprotein were produced in rabbits. The peptide was analogous to amino acid sequences 735 to 752 from the human T cell leukemia virus-IIIB isolate of HIV. Characteristics of the anti-Id preparation included: 1) detection of a shared determinant present on a second chimpanzee and one of three rabbit antibody preparations directed against the synthetic peptide, 2) failure to recognize an idiotype (Id) in BALB/c mouse antisera to the peptide, and 3) partial inhibition of the homologous chimpanzee Id preparation from binding either peptide or a recombinant HIV gp160 preparation. Immunization of BALB/c mice with the anti-Id induced an antipeptide response which bound a recombinant gp160 preparation without subsequent peptide or gp160 exposure. The anti-gp160 containing sera from mice immunized with anti-Id were able to inhibit the Id-anti-Id reaction indicating that an Id-positive antibody response was induced. This Id is not normally expressed in the murine anti-gp 160 immune response to the synthetic peptide and suggests that this anti-Id may activate normally silent clones. This study indicates that Id networks may be operational during the immune response to HIV epitopes. Alternatively, anti-Id may be useful in altering the serologic characteristics of an antibody response to HIV and may offer potential for modulating the immune response in this viral infection.
Interleukin secretion by B cell lines and splenic B cells stimulated with calcium ionophore and phorbol ester.
Authors: Taira S , Matsui M , Hayakawa K , Yokoyama T , Nariuchi H 
Published: December 2022

Abstract
A B cell lymphoma A20.2J and splenic B cells produced an active material to support the proliferation of an interleukin 2 (IL-2)-dependent T cell line, CTLL-2, by stimulation with both calcium ionophore A23187 and phorbol myristate acetate (PMA). Although the production of the active material was induced by stimulation with A23187 alone in A20.2J cells, both A23187 and PMA were essential for the stimulation of splenic B cells. Neither A20.2J cells nor splenic B cells produced the active material by stimulation with PMA alone. The production was inversely proportional to the concentration of fetal calf serum in culture medium. The active material produced by B cells was indicated to be IL-2 and not B cell-stimulating factor 1 (BSF-1) for the following reasons: 1) the proliferation of CTLL-2 cells in the presence of active material was inhibited by the inclusion of anti-IL-2 receptor or anti-IL-2 in culture medium but not by anti-BSF-1; 2) the material showed no co-mitogenic activity to purified splenic B cells with anti-immunoglobulins and did not support the proliferation of FDC-P2 which are known to grow in the presence of BSF-1; and 3) IL-2 mRNA could be detected in A20.2J and splenic B cells stimulated with A23187 and PMA in Northern blot analysis. Some B cell hybridomas were also shown to produce IL-2 by similar stimulation to A20.2J. Splenic B cells as well as A20.2J cells were able to produce IL-2 by stimulation with anti-immunoglobulins. These results suggest that under certain conditions IL-2 can be produced by splenic B cells, at least some subsets of B cells, and B cell lines.
Expression of tumor necrosis factor receptors on human monocytes and internalization of receptor bound ligand.
Authors: Imamura K , Spriggs D , Kufe D 
Published: December 2022

Abstract
Tumor necrosis factor (TNF) is a polypeptide produced by monocytes and macrophages. Although TNF receptors have been identified on a variety of cell types, previous studies have not determined whether these receptors also exist on monocytes. In the present work, highly purified recombinant TNF was labeled with 125I. The 125I-labeled TNF bound specifically to receptors on human monocytes and monocyte membrane preparations. A curvilinear Scatchard plot indicated the presence of TNF-binding sites with two different affinities. The results also indicate that receptor-bound TNF is rapidly internalized by monocytes and then degraded intracellularly. These findings are in concert with recent studies demonstrating that TNF immunomodulates monocyte function by an autocrine mechanism.