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)

1. Among patients transplanted in 93 selected centers with good follow-up data, the 10-year graft survival of first cadaver-donor transplants was 18%, parental donor grafts 39%, and HLA-identical sibling donor grafts 66%. The respective half-lives were 6.8, 10.8, and 24.5 years. The donor relationship has been the most important factor in long-term success. 2. Patient half-life for recipients younger than 16 was 36 years; for recipients 16-50 years old it was 17.6 years, and for those over age 50, it was 10.4 years. This marked difference in patient half-lives severely affected functional graft half-lives for the 3 age groups; 6.8, 10.3, and 16.7 years, respectively. However, the differences in patient survival for the 3 age groups were not significantly reflected in graft half-lives that were 6.8, 7.7, and 6.5 years, respectively. Thus, graft loss resulting from rejection was significantly lower in older than in younger patients. 3. Cadaver-donor kidneys with cold ischemia time up to 12 hours and half-lives of 9.1 years in transplants performed before 1975, compared to half-lives of 6.4 years for those with more than 24 hours cold ischemia time. In transplants performed between 1980 and 1983, the half-life of kidneys with cold ischemia time up to 12 hours was 8.7 years, compared to 6.9 years for those with more than 24 hours cold ischemia time. The long-term effect of cold ischemia persists but has diminished in recent years. 4. HLA-A,B loci matching had a significant effect on long-term graft survival. The 10-year graft survival of A,B matched grafts was 30% compared to 18% for 3 or 4 HLA-A,B mismatched transplants. This difference increased at 15 years to 25% in the matched grafts and 10% in the mismatched grafts. 5. A very strong recipient race effect was evidenced by the 24% 10-year graft survival in Whites compared to 10% in Blacks. The half-lives were 8.2 in Whites and 4.8 in Blacks. 6. A listing of 15-year graft survivors has been compiled according to transplantation centers. There was a total of 969 from cadaver donors, 283 from parental donors, and 457 from sibling donors. 7. An analysis of the characteristics of the 15-year graft survivors showed a preponderance of patients with favorable factors, noted in the analysis above. As might be expected, the most striking was the fact that 27% of the 15-year survivors had received kidneys from sibling donors, despite the fact that such donors comprised only 17% of those transplanted in the pre-1975 era.
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PMID:Fifteen-year kidney graft survival. 248

1. Variation among centers accounted for about one-third of the assignable variation in kidney transplant graft survival. 2. Centers varied systematically in their use of CsA and of pretransplant transfusions and in transplant cold ischemia times--factors strongly related to graft outcome. About 90% of patients received CsA. 3. At some centers, graft survival rates in the low 90% range were attained for first transplants from cadaver donors. 4. Variation among centers was less noticeable at high survival rates. Nearly all centers had good results using HLA-identical sibling donors. 5. Centers with better survival rates tended to treat fewer transplants with CsA. There was a modest, but potentially interesting, negative correlation.
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PMID:Center variability. 248 12

To test the hypothesis that susceptibility to NK cell-mediated cytolysis varies inversely with the levels of target cell class I HLA expression, NK-susceptible K562 and MOLT-4 target cells have been transfected via electroporation with cloned human class I HLA-A2 and HLA-B7 genes. Stably transfected cells expressing varying levels of cell-surface class I HLA have been selected by fluorescent activated cell sorting and tested for susceptibility to NK-mediated cytolysis by freshly isolated peripheral blood NK cells from nine normal volunteers as well as by cloned human NK effectors and tumor cells from a patient with an NK cell lymphoproliferative disorder. Expression of class I HLA did not alter the susceptibility of K562 or MOLT-4 target cells to NK-mediated cytolysis by any of the effectors tested. In addition, the class I HLA-expressing transfectant cells were identical to mock transfected cells in their ability to compete for lysis in cold target inhibition assays. Treatment of both mock-transfected and class I HLA-transfected K562 cells with IFN-gamma resulted in decreased susceptibility to NK-mediated cytolysis which was independent of the total level of class I HLA expression. These results demonstrate that the level of target cell class I HLA expression is not sufficient to determine susceptibility or resistance to NK-mediated cytolysis of the classical NK targets K562 and MOLT-4.
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PMID:Susceptibility to natural killer cell-mediated cytolysis is independent of the level of target cell class I HLA expression. 249 7

We investigated the sensitivity of thyroid epithelial cells (thyrocytes) to IL-2 activated killer cells. The thyrocytes were lysed by autologous and allogeneic IL-2-activated killer cells; there were no differences in sensitivity to the killer cells between normal thyrocytes and thyrocytes from patients with Graves' disease. When thyrocytes were pretreated with recombinant interferon (rIFN) gamma or alpha, the IL-2-activated killer cell-mediated cytotoxicity was depressed and varied inversely with the cell surface expression of class I HLA gene products. The rIFN-gamma pretreatment did not alter the kinetics of thyrocytes lysis by IL-2-activated killer cells. Using cold target competition analysis, rIFN-gamma-pretreated thyrocytes clearly competed less effectively than did untreated cells for lysis of untreated target cells. These results suggest that rIFN-gamma or IFN-alpha pretreatment of thyrocytes may reduce their ability to be recognized by effector cells. These findings suggest that destruction of thyrocytes in autoimmune thyroiditis may be, in part, due to IL-2-activated killer cells and may be regulated by IFN.
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PMID:Cytotoxic activity of interleukin-2 (IL-2) activated killer cells toward thyroid epithelial cells. 250 57

Touraine et al reported some cases lacking HLA-class I antigens on the cell surface of their lymphocytes as "Bare lymphocyte syndrome" (BLS). Recently we experienced a case of BLS the clinical features of which are very similar to those of diffuse panbronchiolitis (DPB). Namely, she had chronic pansinusitis, diffuse nodular shadows on her chest X-ray film, obstructive impairment of pulmonary function tests and continuous increase of cold hemagglutinin titer. The pathogenesis of DPB is not confirmed. However, this case and other cases with sino-bronchial syndrome suggest that patients with DPB may have some immunodeficiencies. In addition the immunosuppressive action of erythromycin and its effectiveness on DPB were interesting. From these points of view, we discussed the relationship between this case and DPB, and the pathogenesis of DPB.
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PMID:[A case of the bare lymphocyte syndrome with clinical manifestations of diffuse panbronchiolitis]. 261 15

1. In the long-term period, the half-life effectively measured loss rate. For HLA-identical sib donors the half-life was 25 years; for parental donors, 13 years; and for cadaver donors, 8 years (now possibly 11 years). 2. HLA-A,B,DR matching exerted the greatest effect on half-life, for a half-life of 17 years was achieved for cadaver donors. This rate was not quite as high as that for A,B,DR matched siblings but was higher than the one haplotype mismatched parental donor transplants. 3. Caucasian recipients had a half-life of 8 years compared to 5 years for black recipients. 4. Excellent centers had a 10-year half-life compared to 5 years for fair centers. 5. Cold ischemia time over 24 hours, recipient age over 55, and donor age of 50-60 had a small effect on the half-life in the order of 1 to 3 years. 6. Among the short-term factors that affect the 1-year graft survival, there was a 12% difference between excellent and fair centers. An 11% difference between A,B,DR matched transplants and 6 A,B,DR mismatched grafts was noted. First-cadaver donor grafts had a 10% higher graft survival at 1-year than second grafts. Other factors together with the difference in 1-year graft survival between the extremes were as follows: sensitization 9%, race 8%, transfusion 6%, donor age 6%, diabetic 3%, recipient age 3% and cold ischemia 1%. Thus more factors affect short-term survival than long-term survival.
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PMID:Long-term survival of kidney grafts. 265 Feb 6

We have derived a number of transgenic mouse lines which express the human major histocompatibility complex class I gene HLA-A2.1. Two lines carry the complete human HLA-A2.1, the others bear a recombinant gene in which the HLA-A2.1 coding regions are fused to the H-2Kb promoter. Analysis of transgenic spleen cells by immunofluorescence demonstrates that these mouse cells express HLA-A2.1 on their surface in association with mouse beta 2-microglobulin (beta 2m), confirming that HLA-A2 does not require human beta 2m to be expressed at the cell surface. The cells contain more HLA mRNA than endogenous H-2 class I mRNA. There is also a large pool of non-beta 2m-associated HLA heavy chain inside the cell. In contrast the amount of HLA:beta 2m complex is low. Thus, in transgenic mice HLA-A2 seems to compete poorly with H-2 heavy chains for mouse beta 2m. The HLA-A2.1 transgenic mice do not produce influenza-virus-specific cytotoxic T cells (CTL) restricted to the HLA transgene, at least in sufficient numbers to be measured in a direct bulk CTL assay. The dominance of H-2-restricted clones may be the result of quantitative rather than qualitative factors. However, HLA-A2.1 transgenic spleen cells are effective in stimulating an allogeneic CTL response in normal mice. This response is not H-2 restricted. Cold target inhibition studies show that there are at least two populations of CTL, one of which is specific for HLA-A2.1 on mouse cells. This result suggests that at least some allo-CTL are directed against major histocompatibility complex plus "self-peptide".
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PMID:Expression and function of HLA-A2.1 in transgenic mice. 267 61

Anti-lymphocytic antibodies (ALA) have been described in a variety of autoimmune disorders. We have investigated the presence of ALA in autoimmune chronic active hepatitis (aCAH) starting in childhood. Using a modified Terasaki technique ALA were found in 17 of 18 patients with aCAH but in only one of 15 patients with alpha-1-anti-trypsin deficiency or Wilson's disease and three of 27 age-matched healthy controls (P less than 0.0005 for both). Sera from 12 patients with uncontrolled aCAH had significantly higher cytotoxicity values than sera from six children with inactive diseases (P less than 0.01). ALA were directed to T but not B lymphocytes and were not reactive with specific HLA antigens. No preferential killing was observed against CD4 or CD8 positive T lymphocytes. Characterization of ALA revealed them to be cold-reactive IgM. The possible role of ALA in aCAH is discussed.
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PMID:Anti-lymphocytic antibodies in autoimmune chronic active hepatitis starting in childhood. 278 29

CTL lines were established in vitro by stimulating patient lymphocytes with autologous melanoma cells in the presence of IL-2. Resulting CTL lines lysed autologous melanoma and failed to lyse several allogeneic melanomas or K562. The mechanism of target cell recognition by autologous tumor-specific CTL was evaluated in this system, using several CTL lines: DT6, DT105, DT141, DT166, DT169, and DT179. Autologous melanoma lysis was inhibited by W6/32, mAb directed against HLA class I Ag, but not by L243, mAb directed against HLA class II Ag. CTL from DT6, DT141, DT166, DT169, and DT179 lysed fresh and cultured allogeneic melanomas, which shared the HLA-A2 Ag, but failed to lyse allogeneic melanomas, which shared B-region or C-region Ag, or shared no HLA class I Ag. CTL from DM141 lysed DM93, which shared A2 and Bw6, but failed to lyse DM105, which shared only Bw6. DM105 CTL failed to lyse allogeneic melanomas that shared HLA-A1, or that shared B or C region Ag, but they did lyse allogeneic melanoma DM49, which expressed an A region Ag that either was A10 or was serologically cross-reactive with A10. A T cell leukemia line, three EBV transformed B cell lines, and a pancreatic cancer line, all of which expressed HLA-A2, were not lysed by DM6 or DM179 CTL. Furthermore, HLA-matched nonmelanomas failed to inhibit autologous tumor lysis in cold target inhibition assays, whereas an HLA-A2+ allogeneic melanoma, DM93, inhibited autologous tumor lysis as effectively as the autologous tumor itself. HLA-A2, and possibly other HLA-A-region Ag, appear to function in HLA-restricted recognition of shared melanoma associated Ag by CTL.
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PMID:The role of HLA class I antigens in recognition of melanoma cells by tumor-specific cytotoxic T lymphocytes. Evidence for shared tumor antigens. 278 41

Antibodies that induce antibody-dependent cellular cytotoxicity (ADCC) of human umbilical-vein endothelial cells (EC) were detected using serum of a renal transplant patient who had experienced a severe vascular rejection episode after receiving an HLA-identical kidney graft from a living-related donor. This reactivity was absent in sera obtained before transplantation. The antibody nature of the reactivity present in the post-transplantation sera was proven by gelfiltration studies, protein A absorption, pepsin-digestion experiments, and incubation with subclass specific monoclonal antibodies; predominantly IgG1 antibodies were found to bind to EC and induce ADCC. The specificity of the antibodies could be shown in panel studies using EC lines of various donors. In order to investigate the clinical relevance and incidence of anti-EC ADCC, we examined whether anti-EC reactivity could be observed in 9 additional renal transplant patients. Sera of 2 of these patients were found positive in the ADCC assay, whereas 20 normal serum donors were negative. ADCC against EC in these patients was not caused by classic antiendothelial-monocyte (EM) antibodies. Using various experimental systems (adherent cell depletion, monoclonal antibody blocking, cold target cell inhibition) it was shown that the natural killer/killer (NK/K) cells present within the peripheral blood mononuclear cell population were responsible for EC lysis. These findings demonstrate that IgG1 antibodies directed against polymorphic non-HLA, non-EM antigens on EC can be induced by renal allotransplantation. Via Fc-receptor interaction with NK/K cells, these antibodies can be responsible for ADCC against EC.
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PMID:Induction of antibody-dependent cellular cytotoxicity against endothelial cells by renal transplantation. 279 23


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