bluuebunny/crossref_metadata_2025_split huggingface dataset:
Growth inhibition of Candida albicans by human polymorphonuclear neutrophils: activation by interferon-gamma and tumor necrosis factor.
Authors: Djeu J Y , Blanchard D K , Halkias D , Friedman H 
Published: December 2022

Abstract
This study was designed to determine whether anti-fungal activity in human polymorphonuclear neutrophils (PMN) might be under the regulation of cytokines such as tumor necrosis factor (TNF) and interferon-gamma (IFN-gamma). By using a radiolabel microassay developed in our laboratory that makes use of the incorporation of [3H]glucose into residual candida, we demonstrated that PMN were better able to inhibit Candida albicans growth in vitro than peripheral blood lymphocytes (PBL). PMN from normal volunteers added to C. albicans for 24 hr at 37 degrees C in a 96-well microplate inhibited fungal growth almost completely at the 300:1 effector/target ratio and frequently at 100:1. Significant activity was still detected at 10:1. In contrast, PBL from the same donors had less activity than PMN at all the ratios tested and lost all function at the 30:1 ratio. TNF and IFN-gamma added to the PMN/candida cultures additionally enhanced PMN to inhibit candida growth. Both cytokines effectively activated PMN down to 0.1 to 0.01 U/ml, and neither cytokine interfered directly with fungal growth, even up to 1000 U/ml. Concentrations of TNF and IFN-gamma below the level that enhanced PMN function when added together to PMN acted synergistically to significantly enhance their anti-fungal activity. Therefore, TNF and IFN-gamma which are active on lymphoid cells, also appear to have the ability to directly activate PMN, and the synergistic action of the two cytokines at low doses that may be below the toxic range may prove to be of clinical importance in protection of immunocompromised host against opportunistic infections.
Synergistic antitumor effect of interferon and anti-idiotype monoclonal antibody in murine lymphoma.
Authors: Basham T Y , Kaminski M S , Kitamura K , Levy R , Merigan T C 
Published: December 2022

Abstract
Both IFN-alpha and anti-idiotype monoclonal antibody therapy have significant antitumor activity in vivo in a murine B cell lymphoma model. Combination therapy with syngeneic anti-idiotype antibody of the IgG2a or IgG2b isotype (a single i.p. injection of 100 micrograms) and recombinant human hybrid interferon-alpha A/D (10(4) to 10(6) U three times weekly for 3 wk) synergistically increased median survival time in mice challenged with a lethal dose of tumor cells compared with the sum of the median survival times of the two individual treatments. IFN-alpha has direct antiproliferative activity against 38C13 in vitro and enhances in vitro macrophage anti-idiotype antibody-specific cytolysis for IgG2a, IgG2b, and IgG1 isotypes.
Relationship among function, phenotype, and specificity in primary allospecific T cell populations: identification of phenotypically identical but functionally distinct primary T cell subsets that differ in their recognition of MHC class I and class II allodeterminants.
Authors: Golding H , Mizuochi T , McCarthy S A , Cleveland C A , Singer A 
Published: December 2022

Abstract
The goal of the present study was to evaluate the relationship among function, Lyt phenotype, and MHC recognition specificity in primary allospecific T cell populations. By using Lyt-2+ and L3T4+ T cells obtained from the same responder populations, we assessed the ability of T cells of each phenotype to generate cytotoxic effector cells (CTL) and IL 2-secreting helper T cells in response to either class I or class II MHC allodeterminants. It was found that a discordance between Lyt phenotype and MHC recognition specificity does exist in primary allospecific T cells, but only in one T cell subpopulation with limited functional potential: namely, Lyt-2+ T cells with cytotoxic, but not helper, function that recognize class II MHC alloantigens. Target cell lysis by these Lyt-2+ class II-allospecific CTL was inhibited by anti-Ia monoclonal antibodies (mAb), but not anti-Lyt-2 mAb, indicating that they recognized class II MHC determinants as their "restriction" specificity and not as their "nominal" specificity even though they were Lyt-2+. A second allospecific T cell subset with limited functional potential was also identified but whose Lyt phenotype and MHC restriction specificity were not discordant: namely, an L3T4+ T cell subset with helper, but not cytotoxic, function specific for class I MHC allodeterminants presented in the context of self-Ia. Thus, the present study demonstrates that primary allospecific T cell populations contain phenotypically identical subpopulations of helper and effector cells that express fundamentally different MHC recognition specificities. Because the recognition specificities expressed by mature T cells reflect the selection pressures they encountered during their differentiation into functional competence, these findings suggest that functionally distinct but phenotypically identical T cell subsets may be selected independently of one another during ontogeny. Thus, the existence of Lyt-2+ CTL specific for class II allodeterminants can be explained by the hypothesis that the association of Lyt phenotype with MHC recognition specificity results from the process of thymic selection that these Lyt-2+ effector cells avoid.
Human monoclonal anti-T cell antibody from a patient with juvenile rheumatoid arthritis.
Authors: Alpert S D , Turek P J , Foung S K , Engleman E G 
Published: December 2022

Abstract
Antibody JRAI is a human monoclonal IgM antibody derived from a patient with juvenile rheumatoid arthritis that is cytotoxic to a subpopulation of normal T lymphocytes. JRAI recognizes approximately 80% of normal peripheral blood T cells, 90% of CD4+ cells, and 75% of CD8+ cells, as determined by complement-mediated cytotoxicity. Within the CD8+ population, JRAI preferentially spares OKM1+ and Leu-11+ cells. These CD8+ cells retain suppressor-effector potential and show enriched natural killer cell activity. Within the CD4+ population, JRAI preferentially kills cells within the Leu-8+ subset, which contains suppressor-inducer cells, and spares the Leu-8- subset, which contains the helpers for immunoglobulin synthesis. JRAI appears to recognize a previously undefined human lymphocyte surface molecule expressed differentially on phenotypically and functionally distinct subsets of human T cells.
HLA-linked nonresponsiveness to Cryptomeria japonica pollen antigen. I. Nonresponsiveness is mediated by antigen-specific suppressor T cell.
Authors: Matsushita S , Muto M , Suemura M , Saito Y , Sasazuki T 
Published: December 2022

Abstract
The objective of this study was to elucidate the cellular mechanism of IgE nonresponse to the Cryptomeria japonica (Japanese cedar) pollen antigen (CPAg), which was shown in our previous study to be HLA-linked (1). We established an assay system for the measurement of small amounts of anti-CPAg IgE antibody, both in an antigen-specific and isotype-specific manner, and a culture system to induce antigen-driven IgE antibody synthesis in vitro. By using these methods, we clarified that the function of the HLA-DR molecule in the CPAg-driven IgE response is similar to that of I-A or I-E molecule in mice, namely the product of immune response genes (Ir-genes), because anti-HLA-DR monoclonal antibody blocked the response, and the interaction between monocyte and monocyte-depleted peripheral blood lymphocytes (PBL) to respond to CPAg was restricted by HLA-DR. Furthermore, PBL from nonresponders revealed a specific IgE response to CPAg when the Leu-2+3- T cell fraction was depleted, thereby suggesting that even nonresponders have Leu-2-3+ T cell and B cell clones specific for CPAg, and they apparently show no response due to the presence of CPAg-specific Leu-2+3- suppressor T cells. This suppressor T cell fraction abolished the IgE response of the autologous B + monocyte + Leu-2-3+ T cell in a CPAg-specific manner. The current cellular analysis together with our previous genetic analysis strongly suggest that the HLA-linked IgE nonresponse to CPAg is mediated by CPAg-specific suppressor T cells. The HLA-linked gene controlling the nonresponsiveness to CPAg is thus designated as the immune suppression gene for CPAg (Is-CPAg). Mapping of Is-CPAg within HLA-DQ subregion is discussed.
The NZB X SWR model of lupus nephritis. II. Autoantibodies deposited in renal lesions show a distinctive and restricted idiotypic diversity.
Authors: Gavalchin J , Datta S K 
Published: December 2022

Abstract
The F1 progeny (SNF1) derived from crossing autoimmune NZB with normal SWR mice uniformly develop lethal glomerulonephritis in marked contrast to the NZB parents. In the preceding paper we found qualitative and idiotypic differences between the anti-DNA antibodies produced by the SNF1 mice and their NZB parents. We identified two clusters of interrelated cross-reactive idiotypic (CRI) families among the SNF1-derived autoantibodies. Here we analyzed the idiotypic profile of the broad spectrum of immunoglobulins deposited in the nephritic kidneys of SNF1 mice and found a restricted idiotypic diversity. To establish that the autoantibody idiotypes detected in the renal lesions were not there as a result of nonspecific trapping, five separate batches of kidney eluates obtained from 100 SNF1 kidneys were analyzed. Both during early and late stages of nephritis, the predominant and consistent idiotypic markers of antibodies in the renal lesion of SNF1 mice were those shared by the two clusters of anti-DNA CRI families. We have termed these nephritogenic idiotypic markers collectively as idiotypes-lupus nephritis-SNF1 or IdLNF1. The Id564 family that encompasses a set of SNF1-derived highly cationic anti-DNA antibodies bearing the normal SWR parent's allotype was more prominently represented in the SNF1 kidneys with early nephritis. Although cationic antibodies were prevalent, the IdLNF1 markers were present on both cationic and anionic or neutral antibodies in the renal lesions of SNF1 mice, and the Ig allotypes of both parents were equally represented in those nephritogenic antibodies. The IdLNF1 positive family of antibodies were also found in high levels in the sera of old SNF1 mice, but they could not be detected in the sera of NZB or SWR mice, nor were they present in the immunoglobulins deposited in the kidneys of rare old NZB mice. The results suggest that select families of nephritogenic idiotypes that are dormant in the autoimmune NZB and the normal SWR parents become expressed in the SNF1 progeny due to genetic and immunoregulatory defects.
Identification of IL 2R+ T cells and macrophages within rejecting rat cardiac allografts, and comparison of the effects of treatment with anti-IL 2R monoclonal antibody or cyclosporin.
Authors: Hancock W W , Lord R H , Colby A J , Diamantstein T , Rickles F R , Dijkstra C , Hogg N , Tilney N L 
Published: December 2022

Abstract
Monoclonal antibodies to lymphokine-induced activation antigens of lymphocytes and macrophages were used to analyze the intragraft events occurring during acute rejection of rat heterotopic cardiac allografts. The cells present during untreated rejection were then compared with those present in situ after immunosuppression with the mouse anti-rat IL 2 receptor (anti-IL 2R) monoclonal antibody ART-18 or cyclosporin (CsA). Untreated rats rejected their grafts within 7 days, whereas rats receiving 10 days of i.v. ART-18 antibody therapy showed graft prolongation to more than 21 days, and rats receiving CsA for 7 days maintained their grafts indefinitely. Untreated rejection was associated with an influx of T (W3/13+) cells and macrophages (ED-1+, ED-2+). Activated mononuclear cells (IL 2R+) were identified within rejecting grafts from day 2, and their numbers peaked on days 4 to 6 when 15 to 20% of infiltrating leukocytes were IL 2R+. Double labeling studies of IL 2R+ cells present at day 6 showed surprisingly that both T cells and macrophages expressed IL 2R. In particular, although 55.8 +/- 6.9% (mean +/- SD) of IL 2R+ cells expressed the pan-T cell antigen 3/13, a similar proportion of IL 2R+ cells (49.8 +/- 8.2%) expressed the macrophage antigen ED-2. Conversely, both T cells and macrophage populations showed heterogeneity in their expression of IL 2R, because 39.2 +/- 12.2% of T cells and 31.0 +/- 13.4% of macrophages were IL 2R+. In addition, inflammatory macrophages at day 6 expressed the A1-3 antigen. Expression of this antigen by macrophages has previously been linked with development of macrophage procoagulant activity, and in this model intragraft inflammatory macrophages were closely associated with widespread deposits of fibrin. By comparison with untreated animals, rats treated with either ART-18 or CsA both lacked detectable IL 2R+ cells during the first 14 days post-transplantation (post-Tx), and showed significantly less cellular infiltration. However, although grafts of CsA-treated animals continued to remain IL 2R- and failed to stain with the macrophage activation marker A1-3, ART-18-treated rats showed increasing infiltration by both IL 2R+ mononuclear cells and A1-3+ macrophages, as well as increasing perivascular and interstitial fibrin deposition, prior to rejection by day 22. These studies document the presence of small number of activated intragraft T cells and macrophages during rat cardiac rejection, and show how CsA, and to a lesser extent anti-IL 2R therapy, inhibit this in situ activation and prolong graft survival. (ABSTRACT TRUNCATED AT 400 WORDS)
Use of the monoclonal antibody 12F1 to characterize the differentiation antigen VLA-2.
Authors: Pischel K D , Hemler M E , Huang C , Bluestein H G , Woods V L 
Published: December 2022

Abstract
A monoclonal antibody, 12F1, has been produced that specifically immunoprecipitates the human cell surface structure VLA-2 from platelets and long-term activated T cells, as well as from fibroblast and neuroblastoma cell lines. Cross-linking studies indicate that the VLA-2 structure exists on the cell surface as a 165,000 Mr heavy chain (alpha 2) in noncovalent 1:1 association with a 130,000 Mr light chain (beta). The monoclonal antibody A-1A5, which reacts with the beta subunit common to all VLA structures, was able to completely preclear VLA-2, indicating that all of the alpha 2 subunit was associated with VLA beta-chain. The specificity of 12F1 for VLA-2 allowed independent immunoprecipitation and flow cytometry analysis of this alpha 2 beta structure separate from any other VLA structures that may have been present such as VLA-1 or free beta-subunit. Subunit dissociation studies were used to demonstrate that 12F1 recognizes an epitope on the alpha 2 chain on VLA-2, which is consistent with the 12F1 specificity for VLA-2 alone among the VLA proteins. Analysis of activated T cells indicated that VLA-2, like VLA-1, is another "very late" appearing T cell activation antigen that arises concurrently with VLA-1 starting at day 7 and increasing through 2 wk. VLA-2 was found on many of the same cells as VLA-1 (inactivated T cells, T cell leukemia cells, fibroblasts, SK-N-SH neuroblastoma cells), but VLA-1 and VLA-2 can be expressed independently, because VLA-2 was also present on VLA-1-negative cells such as HSB and platelets, and VLA-1 was present on VLA-2-negative C8215 cells.
Interleukin 1 releases histamine from human basophils and mast cells in vitro.
Authors: Subramanian N , Bray M A 
Published: December 2022

Abstract
Interleukin (IL 1) preparations from five different sources (human monocyte, LPS-stimulated, purified IL 1 from two different laboratories) and human recombinant IL 1 (HrIL 1) were shown to be capable of directly inducing histamine (HA) release from human basophils (10 to 50% of total cellular HA, depending on the source of IL 1). The release was not due to the medium, pyrogens, or other contaminants. Il 1-induced HA release was dose dependent between 1 to 100 U/ml of IL 1 and 1 to 15 ng/ml of HrIL 1 and was rapid, with a peak release at 15 min. HA release induced by IL 1 was blocked completely by preexposure of cells to IL 1 but was not affected by prechallenge with anti-IgE. Also, preincubation of IL 1 with anti-IL 1 antibody abolished the HA-releasing activity. IL 1-induced HA release was also observed in preparations of human adenoidal mast cells. Our data indicate that it is unlikely that the HA release induced by IL 1 is due to a contamination with HA-releasing factor. This effect of IL 1 provides a mechanism for non-IgE-related local HA release and raises the possibility of a link between cellular immunity and immediate hypersensitivity of potential importance for the pathology of immuno/inflammatory diseases.
Aging and lymphocyte cytoskeleton: age-related decline in the state of actin polymerization in T lymphocytes from Fischer F344 rats.
Authors: Cheung H T , Rehwaldt C A , Twu J S , Liao N S , Richardson A 
Published: December 2022

Abstract
T cell functions are known to decline with age, but the underlying cause of the decline is unclear. Because of the importance of cytoskeletal elements in cellular functions, we examined the content and the state of polymerization of actin in lymphocytes from Fischer F344 rats of four different ages (6, 14, 23, and 31 mo). The cellular actin content was determined by a DNAase I inhibition assay. Our results indicate that the total actin content of spleen lymphocytes did not change significantly with age; however, polymeric actin content, particularly in T cells, decreased with age, which might be a result of the shift from the polymeric actin pool to the monomeric pool. Similar changes also occurred in B cells but to a lesser extent. We conclude that the state of polymerization of lymphocytes changed drastically with age, and that this might be an important factor in the age-related decline in the cellular functions of lymphocytes.
Expression of a recombinant murine IgE in transfected myeloma cells.
Authors: Gritzmacher C A , Liu F T 
Published: December 2022

Abstract
We constructed a recombinant gene encoding an immunoglobulin (Ig) heavy chain consisting of the variable region from the phosphorylcholine (PC)-specific secreting myeloma MOPC167 and the epsilon constant region from SJL mice. This gene, cloned into the shuttle vector pSV2gpt, was transfected into J558L myeloma cells, and stable transformants that expressed the epsilon gene were cloned. The IgE heavy chain in these transformants is associated with the endogenous lambda light chain and is secreted as an intact IgE molecule. However, the secreted IgE does not bind to PC conjugated to bovine serum albumin (PC-BSA). The MOPC167 kappa chain gene was cloned into the shuttle vector pSV2neo and was transfected into the epsilon heavy-chain transformant. Stable transformants were cloned that expressed both the epsilon heavy chain and the kappa light chain. IgE secreted from such a transformant was shown to bind to PC-BSA. Both types of secreted recombinant IgE bound to rat basophilic leukemia (RBL) cells, but only the IgE produced by the cell line transformed with the MOPC167 kappa gene could be cross-linked with PC-BSA to cause serotonin release.
Antigen-presenting T cells. II. Clonal responses of alloreactive and virus-specific self-restricted human cytotoxic T cell responses stimulated by T lymphoblasts.
Authors: Kabelitz D , Enssle K H , Fleischer B , Reimann J 
Published: December 2022

Abstract
The capacity of various stimulator cell types to present alloantigens or viral antigens to resting human CD8+ cytotoxic lymphocyte precursors (CLP) was analyzed in a limiting dilution culture system. Cell sorter-separated T lymphoblasts of both CD4+ and CD8+ phenotypes but not resting T cells were found to efficiently stimulate the clonal development of allogeneic CD8+ CLP. Thus, 5000 CD4+ T lymphoblasts activated as many (one out of 200 to one out of 300) allogeneic CLP as 50,000 peripheral blood mononuclear stimulator cells. This potent stimulator activity was found in CD4+ and CD8+ T lymphoblasts activated by mitogen, anti-T3 monoclonal antibody, or mixed leukocyte reactions. Cytotoxic T cells generated in this system were highly specific for HLA class I antigens. Furthermore, T lymphoblasts infected with mumps virus efficiently induced development of autologous CLP into CTL clones that were virus specific and self-HLA restricted, as shown by split-well analysis. The possible in vivo significance of antigen-presenting T lymphoblasts is discussed.
HLA class II restriction of T helper cell response to cytomegalovirus (CMV). I. Immunogenetic control of restriction.
Authors: Gehrz R C , Fuad S , Liu Y N , Bach F H 
Published: December 2022

Abstract
All three HLA class II families (DR, DQ, and DP) are involved in restriction of helper T cell (Th) recognition of nominal antigens including CMV. Only limited studies have been described previously to determine whether restricting determinants of DR and especially DQ are subtypic to the serologically defined DR and DQ specificities, and to what extent restricting determinants are associated with Dw specificities defined in alloresponses. In the present report, we describe a large number of CMV-specific Th clones derived from two different individuals who are seropositive for CMV. Clones were classified as being DR-, DQ-, or DP-reactive based on blocking with monoclonal antibodies. DR- and DQ-restricted clones were then examined in panel studies using antigen-presenting cells (APC) expressing the Dw subtype of the restricting DR-DQ haplotype, as well as APC expressing different Dw subtypes associated with the serologically defined specificity. Unrelated specificities were also included. Our findings show that not only for DR but for DQ as well, the primary restricting determinants appear to be subtypic to the serologically defined antigen; furthermore, subtype restriction for both DR and DQ is very closely associated with single Dw specificities. In several cases in which cross-reactivity among restricting Dw specificities was observed in association with a given DR or DQ haplotype, a molecular basis could be suggested to explain the cross-reacting determinants. A small minority of the clones appeared to be CMV specific, but was restricted by a determinant(s) that is either monomorphic or minimally polymorphic.
Antibody-induced association between discrete regions of HLA class I and II antigens.
Authors: Russo C , Nepo A , Lanza E , Igarashi M , Ferrone S 
Published: December 2022

Abstract
The anti-HLA-DR + DP monoclonal antibody (MoAb) CR11-462 was unexpectedly found to cross-inhibit the binding to B lymphoid cells of the anti-HLA Class I MoAb CR10-215 and CR11-115. The latter two antibodies recognized the same or spatially close antigenic determinant. The cross-blocking of anti-HLA Class I MoAb CR10-215 and CR11-115 by MoAb CR11-462 reflects neither its contamination by anti-HLA Class I antibodies nor its cross-reactivity with HLA Class I antigens. On the other hand, the cross-blocking appears to reflect redistribution of HLA Class II antigens by the MoAb CR11-462, since the MoAb CR10-215 and CR11-115 are not susceptible to blocking when lymphoid cells are treated with 0.025% glutaraldehyde or are coated with Fab' fragments of the MoAb CR11-462. Furthermore, immunoprecipitates from B lymphoid cells preincubated with the MoAb CR11-462 before solubilization contain HLA Class I antigens. Therefore, these results have shown for the first time an antibody-induced association between discrete regions of HLA Class I and Class II antigens on the membrane of B lymphoid cells.