期刊
JOURNAL OF IMMUNOLOGY
卷 179, 期 4, 页码 2609-2615出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.179.4.2609
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资金
- NIAID NIH HHS [R01 AI044142, R01 AI 44142, R01 AI044142-10] Funding Source: Medline
- NIAMS NIH HHS [R01 AR42527, R01 AR 41974, R01 AR041974-14, R01 AR042527-15, R01 AR041974, R01 AR042527] Funding Source: Medline
Rheumatoid arthritis (RA) is characterized by premature immune aging with accumulation of degenerate T cells deficient for CD28. Gene expression profiling of CD4(+)CD(28-) and CD4+CD28+ T cells to discover disease-promoting activities of CD28- T cells identified expression of CD70 as a most striking difference. Hence, CD70 was significantly more expressed in CD4 T cells from RA patients compared with age-matched controls (p < 0.006). The underlying mechanism was a failure to repress CD70 expression after activation-dependent induction. This defect in RA was not related to differential promoter demethylation. CD70 on bystander CD4+CD28- T cells functioned by lowering the threshold for T cell activation; admixture of CD4+CD28- T cells augmented TCR-induced responses of autologous naive CD4+CD28- T cells, particularly of low-avidity T cells. The data support a model in which CD70 expressed on T cells causes degeneracy in T cell responses and undermines tolerance mechanisms that normally control T cell autoreactivity.
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