Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An OKT3+T4+T8-DR+ lymphocyte line was developed from an Epstein-Barr virus (EBV) seropositive individual by repeated stimulation in vitro with autologous EBV-infected B cells. The T cell population designated E-44 was carried for eight months in the presence of Interleukin-2 and was repeatedly tested for cytotoxicity, proliferation and lymphokine production in response to the autologous and a panel of allogenic B cells. The E-44 cells lysed the autologous lymphoblastoid cell lines (LCL) and allogenic B cell lines sharing the DR6.1 major histocompatibility complex antigen with the lymphocyte donors. The EBV genome-negative lymphoma line BJAB and its two, infected in vitro, EBV-positive sublines were lysed with similar efficiencies. Autologous Staphylococcus aureus protein A (Prot-A) induced B, but not Phytohaemagglutinin (PHA)-induced T blasts were also lysed. It is likely that E-44 recognized an antigenic component derived from the fetal calf serum in association with class II determinants expressed on the B cells. Preincubation of E-44 cells with saturating amounts of OKT3 and Leu3a monoclonal antibodies abrogated the lytic effect on the autologous LCL. Cold target competition experiments demonstrated that, within, the population, the same cells reacted with the autologous Prot-A-induced blasts, the EBV-transformed LCL, and also with Daudi (an EBV genome-positive BL line). Although Daudi was the target which was lysed with the greatest efficiency, the avidity of interaction was highest with the autologous LCL because these cells competed best. Among the cells that were sensitive for the lytic effect, only the autologous LCL and Prot-A-induced B blasts triggered release of detectable amounts of Interleukin-2 and induced proliferation of the culture. The results suggest that the affinity of interaction with the target may be decisive for the triggering of the various T cell functions.
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PMID:T lymphocyte culture established by repeated stimulation with the autologous lymphoblastoid line. MHC class II restricted interactions with B blasts. 644 79

The possibility of obtaining a syngeneic antitumor effect by immunization with normal allogeneic cells was investigated by tests of the lytic activity of peritoneal exudate cells (PEC) of BALB/c mice immunized with lymphoid cells of either a single strain or a pool of six different allogeneic strains on the syngeneic Moloney virus-induced lymphoma YC8 target and on one of its clones designated YC8-D1. Significant cytotoxicity on both targets but not on two other BALB/c lymphomas was obtained with PEC of BALB/c mice singly immunized to the non-H-2-incompatible but H-2-compatible DBA/2 or B10.D2 lymphoid cells. The lack of lysis of YC8 cells by PEC of BALB/c mice immune to B10.A (H-2k,d) suggests that the in vitro killing was restricted by Kd-IEd region products of the major histocompatibility complex. Pool immunization was effective in generating antitumor cytotoxic lymphocytes only when DBA/2 lymphoid cells were included in the pool. The pattern of reactivity of effectors elicited in (BALB/c x DBA/2)F1 and in (BALB/c x B10.D2)F1 mice by immunization with DBA/2 and B10.D2 cells showed that at least two sets of antigens are recognized on YC8 targets, one shared by DBA/2 and B10.D2 tissues and the other expressed by DBA/2 cells only. Cold target blocking experiments indicated that the same effectors recognized non-H-2 antigens of DBA/2 and the cross-reacting YC8 determinants. The antitumor effect was mediated by T-cells, since it was abrogated by treatment of effectors with anti-Thy 1.2 serum plus complement. These data indicate that determinants defined by cytotoxic T-lymphocytes are expressed on the BALB/c lymphoma YC8 and cross-react with non-H-2 antigens of DBA/2 and B10.D2 strains.
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PMID:Alloreactivity and tumor antigens: generation of syngeneic antilymphoma killer lymphocytes by alloimmunization of mice with normal cells. 657 38

Moloney leukemia virus-specific cytotoxic T lymphocytes (CTL), generated by secondary in vitro stimulation of spleen cells with syngeneic virus-infected cells, frequently lysed not only syngeneic virus-infected cells, but also noninfected allogeneic target cells. This phenomenon was studied with B6(H-2b) responder cells and a series of H-2Kb-mutant responder cells. Thus, B6 Moloney-specific CTL lysed noninfected Kb-mutant cells, but not B6 cells, whereas Kb-mutant Moloney-specific CTL lysed noninfected B6 cells and not noninfected cells of the same mutant. Cold-target-inhibition studies showed that the CTL reactions against different allogeneic cells were mediated by different subpopulations of virus-specific CTL: lysis of allogeneic target cells was fully inhibited only by the same allogeneic and by syngeneic virus-infected cells, but not by another allogeneic cell, also lysed by the same effector-cell population. Lysis of syngeneic virus-infected cells could not be inhibited by allogeneic target cells. These data imply that a minority of virus-specific CTL shows cross-reactivity with a given allogeneic target cell. It is concluded that limited amino acid substitutions in the Kb molecule alter the repertoire of Moloney virus-specific CTL, as reflected in alloreactive CTL populations, even though the virus-specific CTL response of B6 and all Kb mutants is mainly Db-restricted. Thus, the development of tolerance to self class-I major histocompatibility complex (MHC) molecules affects the repertoire of self-restricted cytotoxic T cells.
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PMID:Mutations in H-2Kb influence the specificity of alloreactive effector cells included in the repertoire of H-2Db-restricted cytotoxic T lymphocytes against Moloney leukemia virus. 660 Oct 58

Two types of biochemically defined class I major histocompatibility complex (MHC) antigens are found in the rat, RT1.A antigens that are ubiquitously expressed and RT1.C antigens which so far are detectable only on certain cell types, notably B and T lymphocytes. It is shown that the cytotoxic T lymphocyte response to minor H antigens of the LEW strain, including the H-Y antigen, and to TNP-modified syngeneic lymphoid cells is restricted by RT1.A but not RT1.C gene products. This conclusion is based on bulk culture assays including cold target inhibition tests and limiting dilution experiments using recombinants between the RT1a and RT1u haplotypes. The possibility that class I MHC antigens exist which have no major restriction function is discussed.
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PMID:Cytotoxic T lymphocytes of the rat are predominantly restricted by RT1.A and not RT1.C-determined major histocompatibility class I antigens. 661 5

Concanavalin A (Con A)-activated cytotoxic lymphocytes have been investigated, mapping the genetic differences between the P815 target and the effector cells required for cell-mediated lympholysis to occur. The target antigens recognized during the effector phase and the phenotype of the killer cell population(s) were also determined. It was found that Con A could activate a population of primed cytotoxic lymphocytes capable of killing target cells that were identical at the major histocompatibility complex (MHC) but differed at other background genes. Thus, after in vivo priming with DBA/2, B10.D2 lymphocytes cultured with Con A were capable of killing the P815 target. Unprimed B10.D2 cells, however, would not. Studies on the involvement of the MHC indicated that differences in the H-2K through H-2S, as well as differences in H-2D and H-2L alone could cause lysis. This killing could not be accounted for by additional differences at Qa-2, a MHC-linked locus. However, the contribution of other similar non-MHC linked loci could not be excluded. Cold target competition experiments indicated that MHC encoded alloantigens were involved as recognition structures on the target cell surface. Antisera plus complement depletion of cytotoxic effector function demonstrated that the cytotoxic cells had the cell surface phenotypes Thy 1.2+, Lyt 2.2+ and natural killer (NK) 1.1-. We conclude that Con A polyclonally activates population(s) of T cells that express antigen-specific cytotoxicity through clonally distributed recognition receptors intrinsic to their membranes when lectin is omitted from the cytotoxic assay.
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PMID:Lymphocyte-mediated cytotoxicity against allogeneic tumour cells. IV. Fine specificity mapping and characterization of concanavalin A-activated cytotoxic effector lymphocytes. 679 35

Five new histocompatibility antigens, designated secondary B cell or (SB) antigens, have been identified by secondary allogeneic proliferative and cytotoxic responses. The reagents used to define the SB antigents are lymphocytes primed between donors matched for all known HLA antigens. The SB antigens stimulate weak primary allogeneic proliferative responses (a mean relative response of 8%) but strong secondary proliferative responses. Strong secondary cell-mediated cytotoxicity is generated against target antigens that are distinguishable from the SB antigens defined by proliferation. Studies by direct lysis and by cold-target inhibition indicate that these target antigens are preferentially expressed on B cells relative to T cells. The SB antigens segregate with HLA, and the gene(s) encoding the SB1, 3, and 4 antigens maps centromeric to HLA-B. The SB antigens are major histocompatibility antigens not only because they are encoded by major histocompatibility complex (MHC) genes, but also by the functional criteria that the proliferative and cytotoxic responses to SB antigens are not restricted by HLA-DR or HLA-A,-B. Parallel studies of the SB antigens and the DR antigens with respect to: (a) their preferential expression on B cells, (b) their function in secondary allogeneic proliferative and cytotoxic respones, and (c) the location of their structural gene within the MHC. However, the SB antigens and the DR antigens are clearly distinct antigens, because population studies indicate that they can occur independently, and family studies indicate that specific SB antigens segregate with HLA haplotypes having different D and DR specificities. Our data are consistent with the hypotheses that the SB antigens are a new segregant series of B cell alloantigens, and that the SB gene and the DR gene derive from a duplicated ancestral gene.
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PMID:Evidence for a new segregant series of B cell antigens that are encoded in the HLA-D region and that stimulate secondary allogenic proliferative and cytotoxic responses. 696 46

The impact of cold storage of cardiac allografts on expression of major histocompatibility complex antigens and vascular adhesion molecules is not known. We obtained serial endomyocardial biopsy specimens at harvest, on implantation, and approximately 15 minutes after reperfusion from six consecutive human cardiac allografts stored in University of Wisconsin solution. Cold ischemia time was 187 +/- 45 minutes. A fourth endomyocardial biopsy specimen was obtained from the recipients of cardiac allografts 1 week after operation. Expression of major histocompatibility complex antigens and vascular adhesion molecules was studied by immunohistochemistry. The intensity was scored blindly by a semiquantitative method. On vascular endothelial cells, the expression of major histocompatibility complex class I and II antigens was strong; ICAM-1 expression was moderate, and expression of VCAM-1 and ELAM-1 was weak to absent. The expression of these antigens on vascular endothelial cells did not change in sequential biopsy specimens. The expression of major histocompatibility complex class I antigens on myocardial cells was weak and remained unchanged. Myocardial cells did not express major histocompatibility complex class II antigens, ICAM-1, VCAM-1, or ELAM-1 on serial examinations. During cold storage of cardiac allografts in University of Wisconsin solution, the expression of major histocompatibility complex antigens and vascular adhesion molecules on endothelial cells and myocardial cells remains unchanged.
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PMID:Expression of major histocompatibility antigens and vascular adhesion molecules on human cardiac allografts preserved in University of Wisconsin solution. 750 49

To investigate the usefulness of 5-Fluorouracil (5FU) for combination with immunotherapy, we examined the effect of preincubation with 5FU on the susceptibility of a renal cell cancer (RCC) cell line, ACHN, to lymphokine-activated killer (LAK) cells. A 4-h 51Cr release assay showed a remarkable increase in the susceptibility of ACHN cells to LAK cells. Dose response experiments demonstrated that 5FU at concentrations as low as 0.002 microgram/ml increased susceptibility to LAK cells. Presence of 5FU at 2 micrograms/ml but not at 0.2 microgram/ml in media blocked LAK activity induction by IL-2. Furthermore, an adhesion assay showed that preincubation with 5FU did not alter the adhesion of LAK cells to tumor cells nor the expression of intercellular adhesion molecule-1 (ICAM-1), lymphocyte function-associated antigen-3 (LFA-3) or major histocompatibility complex (MHC) class I molecules on tumor cells. Cold target competition did not show any difference between 5FU-treated and untreated competitors. These results suggest that increased susceptibility of RCC cells to LAK cells due to preincubation with 5FU might depend on changes in intrinsic lysability involving a post-binding stage of the lytic cycle.
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PMID:5-Fluorouracil increases susceptibility of renal cell cancer cell lines to lymphokine-activated killer cells: evidence for alteration not at the level of recognition but at a post-binding stage of the lytic cycle. 790 37

Interleukin 10 (IL-10) is a cytokine with a variety of reported effects including inhibition of monocyte major histocompatibility complex (MHC) class II-dependent antigen presentation, type 1 helper T cell cytokine production, and inhibition of T cell proliferation. Herein we report the effect of IL-10 pretreatment on antigen presentation to tumor- and allo-specific CD8+ cytotoxic T lymphocytes (CTL). Prior incubation of human melanoma cells with recombinant IL-10 (rIL-10) for 48-72 h resulted in a dose-dependent, up to 100% inhibition, of autologous CTL-mediated, HLA-A2.1-restricted, tumor-specific lysis. Allo-specific CTL cytotoxicity against Epstein-Barr virus-transformed lymphoblastoid cell lines (LCL) was also inhibited, demonstrating a protective effect also on lymphoid cells. In contrast, IL-10 pretreatment of allogeneic LCL or K562 targets had either no effect or slightly enhanced cytotoxic activity mediated by freshly isolated or IL-2-activated natural killer cells. Flow cytometric analysis with monoclonal antibodies against HLA-A2, or nonpolymorphic determinants of MHC class I proteins, revealed a 20-50% reduction in cell-surface expression, whereas intercellular adhesion molecules 1, and 2, and lymphocyte function-associated antigen 3 levels were not affected. In addition, relative to untreated target cells, IL-10 pretreated tumor cells were unaltered in their capacity to affect CTL-mediated lysis by cold target inhibition, demonstrating that the effect of IL-10 is unrelated to the initial binding of CTL to their targets. These results are compatible with an effect of IL-10 on the MHC class I antigen presentation pathway, and suggest a novel mechanism of immune tolerance, based on escape from CTL-mediated tumor and allo-transplant rejection.
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PMID:Interleukin 10 pretreatment protects target cells from tumor- and allo-specific cytotoxic T cells and downregulates HLA class I expression. 796 10

Urticarial reactions encompass a variety of inflammatory and immunological reactions. In order to clarify specific aspects of these processes, we analyzed the distribution and sequential expression of major histocompatibility complex II (MHC class II) molecules in tissue sections from different types of whealing reactions. Using immunohistochemical techniques and monoclonal antibodies, expression of HLA-DR, HLA-DP, and HLA-DQ was examined on resident and infiltrating cells in different skin cell compartments, comparing early with longer-lasting wheals and lesional with uninvolved skin. Sequential biopsies were studied in cold urticaria (CU). No increase of MHC class II molecule expression was found in early prick test wheals to common inhalant allergens. In CU, however, sequential biopsies demonstrated an up-regulation of MHC class II molecules within 30 min after elicitation. This was more pronounced in longer-lasting urticaria lesions of acute, chronic recurrent and delayed pressure urticaria, with HLA-DR and, to a lesser degree, HLA-DP and HLA-DQ being noted on cell infiltrates, on vascular endothelia and around nerves and sweat glands. Nonelesional skin in these types of urticaria also showed increased MHC class II expression. Longer-lasting urticarial wheals are thus associated with up-regulation of MHC class II molecules on resident and infiltrating cells, suggesting an involvement of these molecules in the pathomechanisms of these types of urticarial lesions.
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PMID:MHC class II antigen expression is increased in different forms of urticaria. 856 93


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