Автоантиген и IL-2 активированные CD4+CD25+T регулировочные клетки движутся для выражения CD8 и являются автоантигенной спецификой в сдерживании экспериментального аутоиммунного энцефаломиелита.
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Tran Giang T, Bedi Sukhandep, Rakesh Prateek, Verma Nirupama D, Carter Nicole, Robinson Catherine M, Al-Atiyah Ranje, Hall Bruce M, Hodgkinson Suzanne J
Аннотация
Оригинал публикации
Autoantigen and IL-2 activated CD4+CD25+T regulatory cells are induced to express CD8 and are autoantigen specific in inhibiting experimental autoimmune encephalomyelitis.
Experimental autoimmune encephalomyelitis (EAE) induced by immunization with myelin basic protein (MBP) is a self-limiting disease model of multiple sclerosis. CD4+CD25+Foxp3+T cells play a role in limiting autoimmune disease but treatment with antigen naïve CD4+CD25+ cells does not reduce EAE. This study examined if in vitro activation by MBP and rIL-2 induced CD4+CD25+Foxp3+ cells that could inhibit EAE. Culture of CD4+CD8-CD25+cells from naïve rats with MBP and rIL-2 induced activated Treg that reduced the severity of clinical EAE and infiltration of CD8+T cells and macrophage into brain stem. CD4+CD25+T cells activated by an irrelevant autoantigen and rIL-2 did not suppress EAE. Resting CD4+CD25+T cells activated by autoantigen and rIL-2 have mRNA for Infgr, Il12rb2, Il5 but not Tbet, Gata3, Ilr5ra or Ifng. These changes in mRNA expression are the markers of Ts1 cells. A proportion of CD4+CD8-CD25+ cells activated by MBP/rIL-2 were induced to express CD8α, CD8β and CD62L. Depletion of CD4+CD8α+CD25+ cells removed the capacity of MBP and rIL-2 activated CD4+CD25+T cells to suppress EAE. This study demonstrated that in vitro activation of CD4+CD8-CD25+ cells by MBP/rIL-2 induced relevant antigen-specific Treg within days, which expressed CD8α, CD8β and CD62L with a Ts1 phenotype and that had greater potency than freshly isolated antigen naive CD4+CD25+Treg in suppressing clinical severity of EAE and immune inflammation in CNS. These findings may guide development of antigen-specific Treg for therapy.