Both CD4+CD25+ and CD4+CD25− Regulatory Cells Mediate Dominant Transplantation Tolerance
نویسندگان
چکیده
منابع مشابه
CD4CD25 Regulatory Cells in Human Peripheral Blood
Thymectomy in mice on neonatal day 3 leads to the development of multiorgan autoimmune disease due to loss of a CDCD25 T cell regulatory population in their peripheral lymphoid tissues. Here, we report the identification of a CD4 population of regulatory T cells in the circulation of humans expressing high levels of CD25 that exhibit in vitro characteristics identical with those of the CD4CD25 ...
متن کاملCD4CD25 Regulatory T Cells Preventing Detrimental Autoimmune Reactions
Objective: Autoimmune diseases will occur when the immune response inflicts damage to tissues in the body. Attempts to overcome this disease have a lot to do but they have not yielded satisfying results. In this study, the function of CD4CD25 regulatory T cells was evaluated for therapeutic potential to prevent the development of autoreactive T
متن کاملBoth CD4(+)CD25(+) and CD4(+)CD25(-) regulatory cells mediate dominant transplantation tolerance.
CD4(+)CD25(+) T cells have been proposed as the principal regulators of both self-tolerance and transplantation tolerance. Although CD4(+)CD25(+) T cells do have a suppressive role in transplantation tolerance, so do CD4(+)CD25(-) T cells, although 10-fold less potent. Abs to CTLA-4, CD25, IL-10, and IL-4 were unable to abrogate suppression mediated by tolerant spleen cells so excluding any of ...
متن کاملSelenium upregulates CD4CD25 regulatory T cells in iodine-induced autoimmune thyroiditis model of NOD.H-2 mice
Selenium (Se) is required for thyroid hormone synthesis and metabolism. Se treatment reduces serum thyroidspecific antibody titers in patients with autoimmune thyroiditis (AIT), but the exact mechanism is not clear. We investigated the effects of Se treatment on CD4+CD25+Foxp3+ regulatory T cells (Treg) in a iodine-induced autoimmune thyroiditis model. NOD.H-2h4 mice were randomly divided into ...
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ژورنال
عنوان ژورنال: The Journal of Immunology
سال: 2002
ISSN: 0022-1767,1550-6606
DOI: 10.4049/jimmunol.168.11.5558