bluuebunny/crossref_metadata_2025_split huggingface dataset:
Endothelial leukocyte adhesion molecule-1 and intercellular adhesion molecule-1 mediate the adhesion of eosinophils to endothelial cells in vitro and are expressed by endothelium in allergic cutaneous inflammation in vivo.
Authors: Kyan-Aung U , Haskard D O , Poston R N , Thornhill M H , Lee T H 
Published: December 2022

Abstract
We have compared the adhesion of 51Cr-labeled eosinophils and neutrophils to cultured human umbilical vein endothelial cell (EC) monolayers that have been stimulated with IL-1, TNF, or LPS. Each agent stimulated the adhesion to EC of both eosinophils and neutrophils in a similar dose- and time-dependent manner. F(ab')2 fragments of mAb 1.2B6 (anti-endothelial leukocyte adhesion molecule (ELAM)-1) and mAb 6.5B5 (anti-intercellular adhesion molecule (ICAM)-1) each inhibited partially, and to a similar extent, eosinophil and neutrophil adhesion to EC monolayers prestimulated with TNF (10 ng/ml) for 6 h. Greater inhibition of both eosinophil and neutrophil adhesion was achieved by combining the effects of mAb 1.2B6 with either mAb 6.5B5 or mAb TS1/18 (anti-CD18). These observations indicate that both ELAM-1 and ICAM-1 are involved in the adhesion of eosinophils and neutrophils to EC stimulated with TNF. In order to determine whether these molecules are expressed in vivo during allergen-induced late phase allergic responses in the skin, human skin biopsies were examined at 6 h after Ag or saline challenge with the use of an alkaline phosphatase-staining technique. Both ELAM-1 and ICAM-1 were expressed with greater intensities in Ag-challenged biopsies, suggesting that these molecules may be involved in granulocyte recruitment in vivo. The similarities we have established between mechanisms of eosinophil and neutrophil adhesion to cytokine-stimulated EC suggests that factors other than differential leukocyte-EC adhesion may be responsible for the selective accumulation of eosinophils at sites of allergic inflammation.
Activation of human complement by IgG antisperm antibody and the demonstration of C3 and C5b-9-mediated immune injury to human sperm.
Authors: D'Cruz O J , Haas G G , Wang B L , DeBault L E 
Published: December 2022

Abstract
To investigate the role of C in the pathogenesis of antisperm antibody (ASA)-mediated infertility, we evaluated the binding and biologic effects of antisperm IgG and autologous C on human sperm. A flow cytometric assay using motile sperm as a target for IgG ASA+ (n = 30) and ASA- (n = 5) sera was developed for the concomitant detection of sperm-bound IgG and the initial (C3d) and terminal (C5b-9) C components on the surface of human sperm. Of the 30 IgG ASA+ sera evaluated by flow cytometry, 15 (50%) and 22 (73.3%) sera were also positive for sperm-bound C3d and C5b-9, respectively. Monomeric IgG purified from C-fixing ASA+ serum was able to bind to sperm and induced deposition of C3 on the sperm surface in the presence of human C. Incubation of motile sperm with C-fixing immune sera resulted in a significant loss (43 to 87%) of motility associated with characteristic C5b-9-induced alterations in sperm morphology leading ultimately to sperm lysis. When motile sperm were cocultured with purified polymorphonuclear leukocytes (PMN) in the presence of C-fixing immune sera, the binding of sperm heads to the PMN resulted in the formation of sperm rosettes, whereas non C-fixing or control sera had no such effect. Transmission electron microscopy of thin sections of the rosettes revealed ingestion of the sperm by the human PMN. These data suggested that 1) antibody bound to sperm is capable of activating autologous C by the classical pathway; 2) binding of both IgG and C proteins initiates C3-mediated sperm binding to PMN and sperm inactivation by deposition of membrane attack complex (MC5b-9) of C; and 3) concomitant detection of sperm-bound IgG, C3d, and C5b-9 may serve as an indicator of C-fixing cytotoxic ASA in the sera of infertile couples.
Clonotypic analysis of anti-acetylcholine receptor antibodies from experimental autoimmune myasthenia gravis-sensitive Lewis rats and experimental autoimmune myasthenia gravis-resistant Wistar Furth rats.
Authors: Zoda T , Yeh T M , Krolick K A 
Published: December 2022

Abstract
A single immunization of Lewis rats with purified acetylcholine receptor (AChR) emulsified in adjuvant typically stimulates the production of oligoclonal AChR-reactive antibodies (as demonstrated by IEF) dominated by the IgG2a subclass, of moderate but clonotypically heterogeneous relative Ag-binding avidity, and capable of inducing symptoms of experimental autoimmune myasthenia gravis. Although similar immunization of Wistar Furth rats produces AChR-reactive antibodies with similar characteristics of clonotypic heterogeneity, avidity, and isotype expression, no detectable signs of AChR-dependent muscle impairment is observed. This contrasts the ability to induce impaired AChR function upon the passive transfer of pre-formed Lewis anti-AChR antibodies into naive Wistar Furth rats, suggesting that disease resistance in this model is not conferred at the level of the AChR itself. Moreover, if more aggressive immunization protocols are used (i.e., multiple injections of AChR), a transient breakthrough of AChR-dependent muscle dysfunction can be induced directly in the Wistar Furth strain indicating that the potential for the production of disease-causing antibodies does exist in the Wistar Furth repertoire. IEF analysis of Wistar Furth anti-AChR antibodies has revealed that hyperimmunization results in modified antibody clonotype expression that might explain changing expression of disease symptoms; however, explanations for the apparent "resistance" of Wistar Furth rats to disease induction are likely to be complex.
T cell receptor alpha and beta gene expression in a murine antigen-specific T suppressor lymphocyte clone with cytolytic potential.
Authors: Heuer J , Degwert J , Pauels H G , Kölsch E 
Published: December 2022

Abstract
The composition of alpha and beta TCR genes was analyzed in a murine BSA-specific Ts cell clone with cytolytic potential. The isolated poly(A)+ mRNA from Ts cell clone BVI/5 was used to construct a cDNA library in the bacteriophage lambda gt11. Full-length cDNA clones specific for TCR alpha and TCR beta genes have been detected and isolated by hybridization with specific oligonucleotide probes. The functional rearranged TCR alpha gene is composed of a member of the V alpha 1 family, the junctional gene J alpha TT11 and C alpha. The gene segments V beta 13, D beta 2.1, J beta 2.4, and C beta 2 form the functional rearranged TCR beta gene. Furthermore, a nonfunctional TCR alpha gene transcript has been detected, where a V alpha 8 gene is rearranged to a so far not described J alpha gene segment (J alpha BVI). A stop codon in its junctional region is responsible for this non-functional transcript. By using Southern blot analysis, the described rearranged TCR genes can be detected in the J alpha junctional region and in the J beta 2 cluster on the genomic DNA level. Immunoprecipitation studies with the KT3 anti-CD3 mAb and flow microfluorimetry analysis with the H57-597 anti-TCR-alpha/beta mAb show that TCR/CD3 complexes are synthesized and expressed on BVI/5 Ts cells. Taken together, the cDNA sequencing data, the protein studies, and the specificity of Ag recognition demonstrate that the BVI/5 Ts cell clone not only transcribes the TCR alpha and beta genes but also expresses a functional BSA-specific receptor.
Expression of a novel nuclear protein in activated and in tat-I expressing T cells.
Authors: Bielinska A , Baier L , Hailat N , Strahler J R , Nabel G J , Hanash S 
Published: December 2022

Abstract
The intracellular events that occur in T lymphoid cells after activation or after infection with HIV-1 are not well defined. In the case of HIV-1 infection, it is unknown whether the tat-I gene, an essential gene for viral replication, affects host cell nuclear factors. Using two-dimensional PAGE, we have identified a novel nuclear protein, designated nuclear protein-28,000 (NP-28), which is induced in Jurkat T cells by stimulation with PMA and/or PHA or ionomycin. This nuclear protein has an apparent molecular mass of 28,000 Da and an isoelectric point of 4.6. Interestingly, Jurkat cells transfected with tat-I express higher levels of NP-28 constitutively, without added stimulation. Incubation of Jurkat cells expressing tat-I with PMA and/or PHA or ionomycin causes superinduction of NP-28. We have therefore identified a novel lymphoid nuclear protein induced by T cell activation that occurs in tat-I expressing cells in the absence of activating agents.
Mechanism of Staphylococcus aureus exotoxin A inhibition of Ig production by human B cells.
Authors: Moseley A B , Huston D P 
Published: December 2022

Abstract
Staphylococcus enterotoxins and toxic shock syndrome toxin 1 are members of a family of exoproteins that are produced by staphylococci and bind specifically to MHC class II molecules. Upon binding to MHC class II molecules, these exoproteins are potent stimulators of T cell proliferation via interaction with specific TCR V-beta segments of both CD4+ and CD8+ T cells. These exoproteins also directly stimulate monocytes to secrete IL-1 and TNF-alpha. Furthermore, these exoproteins have a profound inhibitory effect on Ig production by PBMC. We examined the effects of Staphylococcus enterotoxin A (SEA) on proliferation and Ig production of highly purified human B cells. Our results demonstrated that the binding of SEA to MHC class II molecules on B cells does not alter their ability to proliferate in response to Staphylococcus aureus Cowan strain I (SAC) or to produce Ig in response to SAC plus rIL-2. In contrast, the anti-DR mAb L243 inhibited both B cell proliferation and Ig production. Unable to determine a direct effect of SEA on B cell function, we investigated whether the capacity of SEA to inhibit SAC-induced Ig production by PBMC was T cell-dependent. Our results demonstrated that in the presence of T cells, under appropriate conditions, SEA can either function as a nominal Ag for stimulation of B cell proliferation and Ig production or induce T cell-mediated suppression of Ig production. SEA-induced Ig production required T cell help, which was dependent on pretreatment of the T cells with irradiation or mitomycin C; Ig production was not induced by SEA in the absence of T cells or in the presence of untreated T cells. Furthermore, SEA inhibited Ig production in SAC-stimulated cultures of autologous B cells and untreated T cells; pretreatment of the T cells with irradiation or mitomycin C abrogated SEA-induced inhibition of Ig production. Thus, T cell suppression of SAC-induced Ig production was dependent on T cell proliferation. Similar results were observed with both SEA and toxic shock syndrome toxin 1.
Dextran-conjugated anti-Ig antibodies as a model for T cell-independent type 2 antigen-mediated stimulation of Ig secretion in vitro. I. Lymphokine dependence.
Authors: Peçanha L M , Snapper C M , Finkelman F D , Mond J J 
Published: December 2022

Abstract
We have previously demonstrated that dextran-conjugated anti-IgD antibodies (anti-delta-dex) stimulate high levels of B cell proliferation at concentrations that are 1000-fold lower than that required by unconjugated anti-Ig. We now show that anti-delta-dex may provide a suitable model to study Ig secretion stimulated by soluble T cell-independent type 2 Ag exemplified by TNP-Ficoll. Thus, both TNP-Ficoll and anti-delta-dex stimulate low to undetectable levels of Ig secretion when cultured with resting B cells. Addition of IL-5 or IL-2 stimulated enhanced anti-TNP responses in the presence of TNP-Ficoll, or induced polyclonal Ig secretion in the presence of anti-delta-dex. Both TNP-Ficoll and anti-delta-dex conjugates stimulated Ig production by Percoll-separated low density (partially activated) B cells in the absence of added lymphokines. These findings point to the similarities in the activation requirements of TNP-Ficoll and anti-delta-dex and suggest that dextran-anti-Ig conjugates, which can induce B cell activation irrespective of Ag specificity, may provide a useful model for studying various parameters that characterize the responses to soluble TI type 2 Ag.
A chimeric IL-2/Ig molecule possesses the functional activity of both proteins.
Authors: Landolfi N F 
Published: December 2022

Abstract
An expression vector (pIL-2/IgG1) was constructed with the coding sequence of human IL-2 inserted upstream of the four exons (CH1, hinge, CH2, and CH3) that encode the human IgG1 H chain constant region. Introduction of this vector into a nonsecreting murine myeloma cell line resulted in the production of a chimeric molecule (IL-2/IgG1) consisting of IL-2 attached to the three Ig constant region domains. This molecule was secreted by the transfectant as a homodimer. Functional characterization revealed that the IL-2/IgG1 chimeric molecule exhibited the binding and proliferation-mediating activities of IL-2. On a per molecule basis, IL-2/IgG1 was indistinguishable from human rIL-2 in the ability to induce the proliferation of an IL-2-dependent T cell line. This chimeric molecule also possesses Ig effector function, in that it can mediate the specific lysis of IL-2R-positive cells in the presence of complement. These results demonstrate that it is possible to maintain Ig effector function in molecules ("immunoligands") in which the binding specificity is conferred not by Ig variable regions, but rather, by a ligand of choice.
Kinetics of N-formyl peptide receptor up-regulation during stimulation in human neutrophils.
Authors: Norgauer J , Eberle M , Fay S P , Lemke H D , Sklar L A 
Published: December 2022

Abstract
The kinetics of receptor up-regulation was examined in isolated neutrophils and in whole blood by flow cytometry during cell activation. Stimulation of neutrophils prepared without exposure to LPS with chemoattractants induced fast up-regulation of N-formyl peptide receptors and C receptor type 3 (CR3). Biphasic N-formyl peptide binding curves were detected for saturating concentrations of N-formyl peptide at 37 degrees C. The bulk of the rapid binding during the first 30 to 60 s is attributed to already expressed binding sites whereas the slow binding over the next 3 to 4 min represents a time course of receptor up-regulation. Support for this interpretation comes from conditions under which the number of binding sites and the progress of the binding curves were affected. Cells treated with LPS, which caused expression of internal N-formyl peptide receptors, exhibited rapid, monophasic binding curves with increased total binding. In LPS-untreated, calcium-depleted cells, N-formyl peptide receptor up-regulation was inhibited and rapid, monophasic binding to a smaller total number of expressed sites was observed. Cytochalasin B enhanced the total number of available N-formyl peptide receptors in LPS-untreated but not LPS-treated cells. In both cases binding was rapid and monophasic suggesting that receptors were either fully or rapidly up-regulated. Although not studied in real-time, C receptor type 3 up-regulation was similar to N-formyl peptide receptor up-regulation in response to LPS, or stimulation by N-formyl peptide, C product C5a, leukotriene B4, and platelet-activating factor in isolated cells and in whole blood. After stimulation with formyl peptide, LPS, or C product 5a, the release of vitamin B12-binding protein paralleled up-regulation of receptors. These data indicate that untreated cells up-regulate N-formyl peptide receptors during cell response at a rate of approximately 10,000/min in a calcium-dependent manner whereas LPS-treated cells already express the bulk of their receptors. In cytochalasin B-treated, degranulating cells 30,000 to 50,000 receptors were up-regulated within a minute.
Cytokine release syndrome induced by the 145-2C11 anti-CD3 monoclonal antibody in mice: prevention by high doses of methylprednisolone.
Authors: Alegre M L , Vandenabeele P , Depierreux M , Florquin S , Deschodt-Lanckman M , Flamand V , Moser M , Leo O , Urbain J , Fiers W 
Published: December 2022

Abstract
The hamster mAb 145-2C11 specific for the CD3 complex of murine T lymphocytes shares many properties with OKT3, including the induction of T cell activation. In vivo, the injection of 145-2C11 entails a variety of pathologic changes in relation to the systemic release of cytokines. We tested the effects on this cytokine release syndrome of different doses of methylprednisolone (m-PDS) given at various intervals of time before the 145-2C11 mAb. The administration of high doses of m-PDS (50 mg/kg) 2 to 3 h before the mAb resulted in an almost complete inhibition of the systemic release of TNF-alpha, IL-2, and IL-6. As far as the pathologic changes are concerned, the hypothermia, the acute renal tubular necrosis, and the fatty infiltration of the liver were completely prevented whereas the hypoglycemia was only partially attenuated. The protective effect of m-PDS on the toxicity of 145-2C11 was confirmed by the reduction of the mortality rate among galactosamine-sensitized mice. The inhibition of the release of cytokines by m-PDS did not affect the immunosuppression triggered by 145-2C11 as assessed by the CTL activity against alloantigens measured 48 h after the injection of the mAb. We conclude that the administration of very high doses of glucocorticoids 2 to 3 h before 145-2C11 prevents the release of cytokines and attenuates the acute toxicity of the mAb. Similar protocols could allow mitigation of the cytokine-release syndrome induced by the OKT3 mAb in man.
Properties of murine antibodies from different V region families specific for bromelain-treated mouse erythrocytes.
Authors: Conger J D , Sage H J , Kawaguchi S , Corley R B 
Published: December 2022

Abstract
We have analyzed the combining site diversity of murine antibodies reactive with bromelain-treated mouse RBC (BrMRBC) in B10.A mice. Although several VH and V kappa genes are used to generate antibodies of this specificity, two combinations account for more than 80% of the repertoire from the spleen: VH11/V kappa 9 and VH12/V kappa 4. Antibodies representing these two predominant groups were found to correspond to two previously reported distinct cross-reactive Id families accounting for most of the anti-BrMRBC reactivity in several strains of mice. mAb of the VH11/V kappa 9 type bound the haptens trimethyl-ammonium and phosphorylcholine much more avidly (approximately 1000 fold) than did the VH12/V kappa 4 type antibodies. Both of these haptens represent constituents of phosphatidylcholine, which BrMRBC-specific antibodies are reported to bind. Despite this differential reactivity, members of both the VH11/V kappa 9 and VH12/V kappa 4 antibody groups lysed BrMRBC with similar efficiencies. These data suggest that the two major classes of BrMRBC-specific antibodies have at least partially different specificities and imply that the events that lead to their high frequencies in the CD5+ repertoire may result from different selective forces.
Evidence for functional heterogeneity in IgG Fc-binding proteins associated with group A streptococci.
Authors: Raeder R , Faulmann E L , Boyle M D 
Published: December 2022

Abstract
A number of group A streptococcal isolates have been compared for their nonimmune reactivity with each human IgG subclass, and rabbit, pig, or horse IgG. The results obtained demonstrate considerable heterogeneity in the expression of type II IgG-binding proteins among and within group A isolates. Extraction and analysis of type II IgG-binding proteins from selected strains demonstrate the existence of five functionally distinct IgG-binding proteins. The type IIo IgG binding protein displayed the greatest range of reactivities, binding to all four human IgG subclasses, and rabbit, pig, and horse IgG. A variant of this protein, designated type II'o, bound all four human subclasses and rabbit IgG, but failed to react with pig or horse IgG. A type IIa protein was recovered from certain group A strains which bound human IgG1, IgG2, IgG4, as well as reacting with rabbit, pig, and horse IgG. A functionally related type IIc activity that displayed all of the reactivities of the type IIa protein but did not bind with human IgG2 was also identified. The final functional form of group A IgG-binding protein, the type IIb protein, bound exclusively to human IgG3. Comparison of these functionally different type II IgG-binding proteins demonstrated no simple structure-function relationship. These studies underscore the heterogeneity of type II Ig-binding proteins expressed by different group A streptococci and document that a single strain can change its pattern of expression of type II IgG-binding protein both quantitatively and qualitatively.
Egg deposition is the major stimulus for the production of Th2 cytokines in murine schistosomiasis mansoni.
Authors: Grzych J M , Pearce E , Cheever A , Caulada Z A , Caspar P , Heiny S , Lewis F , Sher A 
Published: December 2022

Abstract
To characterize Th cell populations induced by helminth infection, spleen cells from mice infected with Schistosoma mansoni were stimulated with parasite (worm or egg Ag) or mitogen (Con A) and the supernatants assayed for the Th1-specific cytokines IFN-gamma and IL-2 and the Th2-specific cytokines IL-4 and IL-5. Th2 cytokine production was not detected in substantial quantity until the 6 to 8th wk of infection and after reaching peak levels at 8 to 12 wk declined slowly thereafter. The time courses of IL-4 and IL-5 production, whereas differing from each other, closely resembled corresponding published data on IgE and peripheral blood eosinophil levels during murine schistosome infection. In contrast, Th1 cytokine responses occurred only during the first 6 wk of infection and were virtually absent during the peak period of Th2 production. To assess the role of egg deposition in the observed pattern of Th response, cytokine production was assayed in mice carrying unisexual schistosome infections in which parasite eggs are absent. Splenocytes from these animals displayed only marginal Th2 cytokine synthesis but greater Th1 cytokine responses than the corresponding cells from mice with bisexual infections. Moreover, cultures of liver tissue or isolated granulomas from infected mice constitutively produced high levels of IL-4 and IL-5 but failed to synthesize significant amounts of IL-2 and IFN-gamma even when stimulated with egg Ag or mitogen. Taken together the data indicate that egg deposition is the major stimulus of Th2 cytokine response in S. mansoni-infected mice and suggest that T cells belonging to this subset must play a major role in egg granuloma formation.