Bibliographic Details
| Title: |
Apaf1 plays a negative regulatory role in T cell responses by suppressing activation of antigen-stimulated T cells. |
| Authors: |
Tong, Honglian1, Miyake, Yasunobu1, Mi-ichi, Fumika1, Iwakura, Yoichiro2, Hara, Hiromitsu1, Yoshida, Hiroki1 yoshidah@cc.saga-u.ac.jp |
| Source: |
PLoS ONE. 3/29/2018, Vol. 13 Issue 3, p1-16. 16p. |
| Subject Terms: |
*APOPTOTIC protease-activating factor 1, *T cells, *APOPTOSIS, *MITOCHONDRIAL pathology, *EMBRYOLOGY, *IMMUNE response |
| Abstract: |
Apaf1 is a critical component of the apoptosome and initiates apoptosis downstream mitochondrial damages. Although the importance of Apaf1 in embryonic development was shown, the role of Apaf1 in immune responses, especially T cell responses, has yet to be elucidated. We generated T cell-specific Apaf1-deficient mice (Lck-Cre-Apaf1f/f mice) and examined the antigen-specific delayed-type hypersensitivity (DTH). Lck-Cre-Apaf1f/f mice exhibited exacerbation of DTH responses as compared with Apaf1-sufficient control mice. In Lck-Cre-Apaf1f/f mice, antigen-specific T cells proliferated more, and produced more inflammatory cytokines than control T cells. Apaf1-deficient T cells from antigen-immunized mice showed higher percentages of activation phenotypes upon restimulation in vitro. Apaf1-deficient T cells from naive (non-immunized) mice also showed higher proliferation activity and cytokine production over control cells. The impact of Apaf1-deficiency in T cells, however, was not restored by a pan-caspase inhibitor, suggesting that the role of Apaf1 in T cell responses was caspase-independent/non-apoptotic. These data collectively demonstrated that Apaf1 is a negative regulator of T cell responses and implicated Apaf1 as a potential target for immunosuppressive drug discovery. [ABSTRACT FROM AUTHOR] |
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