期刊
SCANDINAVIAN JOURNAL OF IMMUNOLOGY
卷 55, 期 6, 页码 546-559出版社
WILEY
DOI: 10.1046/j.1365-3083.2002.01086.x
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资金
- NIAID NIH HHS [R01 AI48805] Funding Source: Medline
The genetic basis and familial clustering of autoimmunity suggest that common phenotypic traits predispose individuals to disease. We found a hyporesponsive T-cell phenotype that was shared by all autoimmune-prone mouse and rat strains tested, including MRL, nonobese diabetic (NOD), NZB, NZW, NZB/W F-1 , SJL and SWR mice, as well as DA and BB rats, but was not evident in nonautoimmune-prone rodents. This T-cell intrinsic, age-independent hyporesponsiveness is measured as an increased activation threshold for upregulation of activation markers upon T-cell receptor (TCR) cross-linking both in vitro and in vivo . Inefficient deletion of CD4 and CD8 single-positive, heat stable antigen (HSA)(hi) medullary thymocytes was also observed in hyporesponsive donors. We interpret these data to suggest that increased TCR-mediated signalling thresholds in autoimmune-prone individuals may contribute to the escape of autoreactive thymocytes from negative selection.
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