bluuebunny/crossref_metadata_2025_split huggingface dataset:
Recognition of HLA class I molecules by antisera directed to synthetic peptides corresponding to different regions of the HLA-B7 heavy chain.
Authors: Choppin J , Metzger J J , Bouillot M , Briand J P , Connan F , Van Regenmortel M H , Levy J P 
Published: December 2022

Abstract
Antisera have been prepared in rabbits and in mice against different peptides corresponding to four hydrophilic and variable regions of HLA-B7 heavy chain (65-82, 99-118, 138-157, and 164-187). Specific antipeptide sera have been obtained with all synthetic peptides; for three of them which were more than 20 amino acids long, highly potent sera were elicited by injection of the free peptide. Three overlapping peptides included in region 138-157 have been used, and two different antigenic sites were detected in this region. HLA molecules solubilized in nonionic detergent were precipitated by antipeptide sera directed against regions 65-82, 138-157, and 164-187, but not by antipeptide serum directed against the less hydrophilic region 99-118. Analysis by two-dimensional electrophoresis of the isolated molecules confirmed the anti-HLA specificity of the antipeptide 65-82 and 138-157 sera. Variable numbers of HLA-related spots were found according to the antisera used. Antipeptide 138-157 serum precipitated numerous HLA molecules and therefore probably reacted with monomorphic determinants whereas antipeptide 65-82 appeared specific for a more limited number of HLA antigens. Such reagents directed against well-defined regions of the HLA class I heavy chain are of considerable interest, notably for the mapping of antigenic epitopes on the molecule and for the study of relationships between structure and function.
Biochemical analysis suggests distinct functional roles for the BLAST-1 and BLAST-2 antigens.
Authors: Thorley-Lawson D A , Swendeman S L , Edson C M 
Published: December 2022

Abstract
The biochemical processing of the BLAST-1 and BLAST-2 activation antigens has been studied. Both are glycoproteins that derive from different precursors of the same apparent m.w. on SDS-PAGE. BLAST-1 is synthesized as a 43,000 m.w. light chain in association with a second heavier chain of 55,000 m.w. The light chain acquires sialylated O-linked glycans and is stably expressed at the cell surface with a half-life of 14 hr. BLAST-2 is also synthesized as a 43,000 m.w. precursor, but it acquires only unsialylated N-linked glycans. The mature glycoprotein is only expressed briefly at the cell surface (half-life of 1 to 2 hr), and is then shed into the culture supernatant as a soluble 33,000 m.w. derivative. The different fates of these molecules, one stably expressed at the cell surface and one shed, suggest disparate roles for these two antigens in B cell activation.
Binding and catabolism of aggregated immunoglobulins containing C3b by U937 cells.
Authors: Mehta R L , Takahashi H , Rudick R A , Knutson D W 
Published: December 2022

Abstract
We studied Fc receptor and C3b receptor (CR1) function on U937 cells, a human monocyte cell line. C3b was incorporated into stable soluble heat aggregates of 125I-IgM (A-IgM) and 125I-IgG (A-IgG) by using functionally pure classical pathway components. C3b incorporation was verified by the ability of aggregates to bind to human red cells and by cosedimentation of 125I and 131I during ultracentrifugation. Cell uptake and degradation of A-IgG X C3b was increased up to twofold compared with A-IgG not containing C3b molecules. However, A-IgG X C3b bound to CR1 after Fc receptors were blocked with nonradiolabeled A-IgG were also not endocytosed and catabolized. Moreover, A-IgM X C3b was bound but not degraded by U937 cells. As expected, uptake of A-IgM without C3b was negligible. CR1-mediated binding of A-IgM X C3b was specifically inhibited both by a murine monoclonal antibody against the human CR1 that blocks C3b binding and by C3b oligomers generated by trypsin activation of C3, but not by monoclonal antibodies against the iC3b receptor (CR3). We conclude that CR1 on U937 cells cause increased binding of A-IgG, and this increased binding leads to increased Fc-mediated endocytosis and catabolism of model immune complexes. However, binding of soluble ligands by CR1 alone, even when binding is multivalent, does not lead to endocytosis and degradation of soluble ligands bearing C3b.
Cells with natural killer activity in the cerebrospinal fluid of normal mice and athymic nude mice with acute Sindbis virus encephalitis.
Authors: Griffin D E , Hess J L 
Published: December 2022

Abstract
Sindbis virus causes an acute, nonfatal inflammatory encephalitis in weanling BALB/c mice. Mononuclear inflammatory cells are present in the cerebrospinal fluid (CSF) as well as in the parenchyma of the brain. Both aspects of this inflammatory response were eliminated by treatment with cyclophosphamide. Athymic nude (nu/nu) mice developed no inflammation in the brain, but did develop a CSF pleocytosis that peaked on day 2 after infection. The time course of the appearance of cells in the CSF was earlier in nu/nu mice than their heterozygote (nu/+) littermates. The pleocytosis in nu/nu mice reached a peak on day 2, whereas in nu/+ mice the peak was on day 4, as it is in normal BALB/c mice. To determine whether some of the CSF cells in nu/nu mice may be natural killer (NK) cells, NK activity was measured in a 4-hr assay by using a YAC-1 target cell. NK cell activity in the spleen and peripheral blood was induced by infection with Sindbis virus in nu/nu mice with a similar time course to that of nu/+ mice (peak 1 day after infection). CSF from nu/nu mice had NK activity present 2 days after infection that was greater than that present in either the peripheral blood or spleen. BALB/c and nu/+ mice had insufficient cells present for assay at day 2, but BALB/c mice had NK activity present in the CSF 3 and 5 days after infection that exceeded that in the peripheral blood or spleen. Brain interferon was detectable on day 1 in nu/nu mice, but not until day 2 in nu/+ mice even though the amounts of brain virus were the same in the two groups at all time points. It is concluded that cells with NK activity contribute to the CSF pleocytosis induced by acute Sindbis virus encephalitis.
The role of T cell accessory molecules in the generation of class II-specific xenogeneic cytolytic T cells.
Authors: Greenstein J L , Foran J A , Gorga J C , Burakoff S J 
Published: December 2022

Abstract
In the generation of allogeneic, hapten-modified and virus-specific cytotoxic T cell (CTL) responses there is usually a requirement for T-T interaction between the T helper cell (TH) and the precursor CTL (CTL). We have investigated the role of a TH signal in the induction of a xenogeneic mouse antihuman CTL response by using membranes and liposomes bearing the xenogeneic antigen to stimulate primed responders. The TH signal can be achieved by either an Ia-restricted, L3T4+ DR-specific T cell or by the addition of nonspecific T helper factors(s). This signal is delivered to an Lyt-2+, L3T4-DR-specific CTL to generate active xenogeneic (xeno-) CTL. The roles of the T cell accessory molecules L3T4, Lyt-2, and LFA-1 in the generation of and target cell lysis by xeno-CTL are investigated.
Multiple epitopes in a dodecapeptide of myelin basic protein determined by monoclonal antibodies.
Authors: Price J O , Whitaker J N , Vasu R I , Metzger D W 
Published: December 2022

Abstract
Three custom synthesized myelin basic protein (MBP) peptides, bovine peptide 79-88, human peptide 80-89, and human peptide 82-91, were used to produce four murine monoclonal antibodies (MAb) that were selected on the basis of reaction in a solid phase radioimmunoassay (SRIA) with human MBP. The MAb were compared with respect to antigen specificity against intact MBP and 10 overlapping MBP peptides. One MAb recognized an epitope near the amino-terminus of bovine MBP peptide 79-88. A second MAb was directed towards an epitope that is more reactive in human MBP peptide 45-89 than in intact MBP, but is not recognized in any of the small MBP peptides examined. The third MAb detected an epitope near the middle of human MBP peptide 80-89, whereas the fourth MAb reacted with the carboxyl-terminal portion of human MBP peptide 82-91. Epitopes recognized in SRIA were sometimes not detected by the same MAb in a fluid phase double antibody radioimmunoassay. These results demonstrate the multiplicity of potential epitopes in a dodecapeptide of MBP and do not support the concept of a single, dominant epitope in the region of MBP peptide 80-89.
Binding and cross-linking of recombinant mouse interferon-gamma to receptors in mouse leukemic L1210 cells; interferon-gamma internalization and receptor down-regulation.
Authors: Wietzerbin J , Gaudelet C , Aguet M , Falcoff E 
Published: December 2022

Abstract
Recombinant E. coli-derived murine IFN-gamma (Mu-rIFN-gamma; 5 X 10(7) U/mg) was radiolabeled with 125I by the chloramine-T method without loss of its antiviral activity. The 125I-Mu-rIFN-gamma showed specific binding to L1210 cells. Scatchard analysis indicates about 4000 binding sites per cell and an apparent Kd of 5 X 10(-10)M. Binding of 125I-Mu-rIFN-gamma to cells was inhibited by both natural (glycosylated) and rIFN-gamma, but not by IFN-alpha/beta. Receptor-bound 125I-Mu-rIFN-gamma was rapidly internalized when incubation temperature was raised from 4 degrees C to 37 degrees C. On internalization, almost no IFN-gamma degradation was observed during 16 hr incubation. 125I-Mu-rIFN-gamma binding capacity decreased in cells preincubated with low doses of unlabeled Mu-rIFN-gamma, but not with IFN-alpha/beta. This receptor down-regulation was dose-dependent: 90% reduction of 125I-Mu-rIFN-gamma binding was observed after preincubation with 100 U/ml. After removal of IFN-gamma from the culture medium, the binding capacity increased with time. However, reappearance of receptor was completely blocked by cycloheximide or tunicamycin, suggesting that re-expression of receptors is not due to recycling but to the synthesis of new receptors, and that the receptor is probably a glycoprotein. Cross-linking of 125I-Mu-rIFN-gamma to surface L1210 cell proteins by using bifunctional agents yielded a predominant complex of m.w. 110,000 +/- 5000. Thus, assuming a bimolecular complex, the m.w. of the receptor or receptor subunit would be close to 95,000 +/- 5000. The formation of such a complex appeared highly specific on the basis of the following criteria: it could be inhibited by the addition of Mu-rIFN-gamma but not by Mu-rIFN-alpha/beta, it was not obtained in cells pretreated with IFN-gamma to induce down-regulation of IFN-gamma receptors, and it was also identified in the IFN-alpha/beta-resistant L1210R cell line, known to be sensitive to IFN-gamma and which we have recently shown to express IFN-gamma receptors.
Histamine-induced suppressor factor inhibition of NK cells: reversal with interferon and interleukin 2.
Authors: Nair M P , Cilik J M , Schwartz S A 
Published: December 2022

Abstract
Culture supernatants of lymphocytes stimulated with 10(-3) to 10(-8) M histamine contain histamine-induced soluble suppressor factor (HISSF) that significantly inhibits the natural killer (NK) cell functions of allogeneic lymphocytes. Lymphocytes precultured with increasing concentrations of HISSF showed a dose-dependent suppressive effect on their NK activity. HISSF was not cytotoxic itself and produced suppressive effects on PBL, NK-enriched large granular lymphocytes (LGL), and isolated T cells. Suppression was evident throughout a range of effector:target cell ratios. Production of HISSF was specifically blocked by the H2 antagonist cimetidine, but not by the H1 antagonist clemastine fumarate. Furthermore, H1 and H2 antagonists themselves do not induce production of HISSF. Although HISSF could inhibit the cytotoxicity of LGL, LGL themselves do not produce HISSF. HISSF inhibition of NK activity could be completely reversed by treating effector lymphocytes with recombinant interferon-alpha (IFN) for 1 or 2 hr or culturing them with purified interleukin 2(IL 2) for 36 hr. Our data suggest that exogenous IFN and IL 2 may have therapeutic potential in the treatment of immunological diseases associated with histamine-induced suppressor cell activity.
Production of interleukin 1 by human endothelial cells.
Authors: Miossec P , Cavender D , Ziff M 
Published: December 2022

Abstract
Vascular endothelial cells (EC) play an important role in the emigration from the blood of the mononuclear cells that participate in the chronic inflammatory response. Because EC express a number of functions of cells of the monocyte/macrophage lineage, EC culture supernatants (ECSN) were examined for the presence of IL 1. In these supernatants, IL 1 activity was low when EC were cultured in the presence of serum. The low level of activity appeared to be due to the spontaneous production by the EC of inhibitors of the thymocyte proliferation assay of IL 1, of 70 kd and 9 kd, as measured by AcA Ultrogel filtration. When EC were cultured in the absence of serum, IL 1 activity was easily demonstrated in crude supernatants. Upon stimulation with LPS, the amounts of IL 1 activity were greatly increased. The release of IL 1 was an early event, detectable after 1 hr of incubation and reaching a maximum after 24 hr. The IL 1 activity produced by EC demonstrated a number of similarities to that of IL 1 produced by monocytes. On AcA 54 gel filtration, as with monocyte-derived IL 1, the IL 1 activity was found in two peaks of 50 to 60 kd and 16 to 18 kd. Upon chromatofocusing of the 16 to 18 kd peak, three active fractions were found, eluting near pH 7.0, 5.6, and 5.0. In addition, when LPS-stimulated ECSN and purified monocyte-derived IL 1 were incubated with a rabbit anti-IL 1 antibody, a parallel reduction in thymocyte-stimulating activity was observed, suggesting that the active agent in ECSN shared a common antigenic site with IL 1. The demonstration of IL 1 production by EC provides additional evidence that these cells, in addition to their functions as vascular cells, may also participate in some of the immune and nonimmune functions previously ascribed to macrophages.
Enhancement of plasma levels of biologically active leukotriene B compounds during anaphylaxis in guinea pigs pretreated by indomethacin or by a fish oil-enriched diet.
Authors: Lee T H , Israel E , Drazen J M , Leitch A G , Ravalese J , Corey E J , Robinson D R , Lewis R A , Austen K F 
Published: December 2022

Abstract
The changes in arterial plasma concentrations of immunoreactive leukotriene B (LTB) were compared after antigen challenge of two groups of sensitized, mepyramine-treated, and mechanically ventilated guinea pigs, one fed a diet enriched with fish oil and the other a control diet enriched with beef tallow. The lung tissue of animals fed a fish oil-enriched diet (FFD) for 9 to 10 wk incorporated eicosapentaenoic acid (EPA) and docosahexaenoic acid to constitute 8 to 9% of total fatty acid content, whereas these alternative fatty acids constituted less than 1% of the total fatty acid content of the lung tissue of animals on a beef tallow-supplemented diet (BFD). The maximum increase after antigen challenge in immunoreactive LTB4 from 0.16 +/- 0.04 ng/ml to 0.84 +/- 0.25 ng/ml in BFD animals and from 0.47 +/- 0.11 to 5.1 +/- 1.4 ng/ml immunoreactive LTB (LTB4 and LTB5) in FFD animals was significant (p less than 0.02) for each. Furthermore, the increase in total immunoreactive LTB in mepyramine-treated FFD animals was significantly greater than the increase in LTB4 in mepyramine-treated BFD guinea pigs at 2 to 8 min after antigen challenge (p less than 0.05). Resolution of arterial plasma immunoreactive LTB from pooled samples by reverse-phase high-performance liquid chromatography demonstrated that the sum of LTB4 and LTB5 in FFD animals exceeded that of LTB4 in BFD animals and that the quantity of LTB4 in the FFD animals was at least as great as that in the BFD animals during anaphylaxis. The products eluting at the retention times of LTB4 and LTB5 exhibited the chemotactic activity of their respective synthetic standards. The combination of indomethacin and mepyramine markedly augmented the antigen-induced increase in arterial plasma immunoreactive LTB4 concentrations in BFD animals, but had no effect on immunoreactive LTB levels in FFD animals. Limited in vivo measurements showing a lesser increase of plasma immunoreactive thromboxane B2 in the FFD relative to the BFD animals during anaphylaxis and ex vivo measurements showing a decreased LTB4-stimulated (cyclooxygenase product-dependent) contractile response of pulmonary parenchymal strips from the FFD relative to the BFD animals provide evidence for blockade in the cyclooxygenase pathway in the FFD animals. The measurements of arterial plasma LTB indicate that indomethacin treatment alone, which inhibits cyclooxygenase activity, and FFD treatment each augment the metabolism of arachidonic acid by the 5-lipoxygenase pathway in animals pretreated with mepyramine.(ABSTRACT TRUNCATED AT 400 WORDS)
Selective augmentation by recombinant interferon-gamma of the intracellular content of S-adenosylmethionine in murine macrophages.
Authors: Bonvini E , Hoffman T , Herberman R B , Varesio L 
Published: December 2022

Abstract
Treatment of mouse peritoneal macrophages with IFN-gamma augmented the intracellular content of S-adenosylmethionine, as measured by quantitative high-performance liquid chromatography. Accumulation of S-adenosylhomocysteine, a competitive product of S-adenosylmethionine, was not detectable, either by direct measurement of absorbance or by radioisotopic techniques in IFN-gamma-treated macrophages. However, accumulation of S-adenosylhomocysteine was observed after treatment of macrophages with known inhibitors of S-adenosylhomocysteine catabolism. No inhibition of phospholipid methylation was observed upon IFN-gamma treatment, indicating that no reduction of the S-adenosylmethionine to S-adenosylhomocysteine ratio is induced by IFN-gamma in murine macrophages. The increased content of S-adenosylmethionine was associated with the acquisition of tumoricidal activity by macrophages upon IFN-gamma treatment. LPS also augmented the cellular content of S-adenosylmethionine and activated macrophages to become cytotoxic, suggesting a common mechanism of action for IFN-gamma and LPS in macrophage activation. Treatment of macrophages with cycloleucine, an agent that induces depletion of cellular S-adenosylmethionine, made the macrophages refractory to induction of cytolytic activity by IFN-gamma, suggesting a critical role for S-adenosylmethionine in macrophage activation.
S-antigen-specific rat T cell lines recognize peptide fragments of S-antigen and mediate experimental autoimmune uveoretinitis and pinealitis.
Authors: Gregerson D S , Obritsch W F , Fling S P , Cameron J D 
Published: December 2022

Abstract
Two S-antigen-specific rat T cell lines expressing the T helper cell surface phenotype (W 3/25+, OX 8-) have been isolated from the spleen and lymph node cells of retinal S-antigen-immunized Lewis rats, one of which displayed neither clinical nor histopathologic signs of experimental autoimmune uveoretinitis. The other rat had recovered from severe experimental autoimmune uveoretinitis for 2 mo before isolation of the cell line. Both lines are specific for S-antigen presented by histocompatible antigen-presenting cells, and also respond in vitro to several of the peptides produced by cyanogen bromide cleavage of bovine retinal S-antigen. The lesions induced by the i.v. transfer of from 1 to 10 X 10(6) viable line cells involve the retina and pineal gland, as is found when Lewis rats are immunized with immunopathogenic doses of S-antigen. Histologic examination of the eyes and pineal glands revealed pathologic lesions typical of experimental autoimmune uveoretinitis, and consisted of marked infiltration of the retina and surrounding tissues and the pineal gland by lymphocytes and inflammatory cells. T cells capable of mediating autoimmune disease are clearly present and readily isolated from both asymptomatic and convalescent animals. No significant differences in specificity for the cyanogen bromide peptides of S-antigen or cell surface phenotype were found in the T cell lines isolated from these two rats, nor was any difference found in the specificity or titer of serum antibodies taken from the original rats for the cyanogen bromide peptides of S-antigen.
Lymphokines regulate immunoglobulin isotype expression in an antigen-specific immune response.
Authors: Tesch H , Müller W , Rajewsky K 
Published: December 2022

Abstract
The control of immunoglobulin class switching appears to involve T cell-derived lymphokines. Such lymphokines have been shown to affect isotype expression in polyclonally activated B cells. We show in this paper that the same lymphokines similarly control isotype expression in an antigen-specific response acting in concert with a "T cell independent" antigen. In this situation, B cell growth factor II (BCGF II) enhances the production of antigen-specific IgM antibodies, whereas the production of antigen-specific IgG1 antibodies is only observed in the presence of B cell differentiation factor gamma (BCDF gamma). These results suggest that these lymphokines (and perhaps additional ones) are involved in the control of isotype expression in antigen-specific responses.
Immunologic activity of lipopolysaccharides released from macrophages after the uptake of intact E. coli in vitro.
Authors: Duncan R L , Hoffman J , Tesh V L , Morrison D C 
Published: December 2022

Abstract
Lipopolysaccharides (LPS) have been isolated from culture supernatants and from cell lysates after the in vitro phagocytosis of E. coli by murine macrophages. By using E. coli radiolabeled specifically in the LPS component with [3H]galactose, our studies have shown that the macrophage-"processed" LPS is enhanced with respect to its immunostimulatory activity in comparison with control phenol-water-extracted LPS. As assessed by its ability to induce interleukin 1 production in naive macrophages or proliferation in cultures of murine splenocytes, the macrophage-processed LPS is between 10- and 100-fold greater in specific activity. Evidence is presented for both structural and chemical alterations in the LPS macromolecule.