Myocardial Infarction Primes Autoreactive T Cells through Activation of Dendritic Cells.

ABSTRACT: Peripheral tolerance is crucial for avoiding activation of self-reactive T cells to tissue-restricted antigens. Sterile tissue injury can break peripheral tolerance, but it is unclear how autoreactive T cells get activated in response to self. An example of a sterile injury is myocardial infarction (MI). We hypothesized that tissue necrosis is an activator of dendritic cells (DCs), which control tolerance to self-antigens. DC subsets of a murine healthy heart consisted of IRF8-dependent conventional (c)DC1, IRF4-dependent cDC2, and monocyte-derived DCs. In steady state, cardiac self-antigen α-myosin was presented in the heart-draining mediastinal lymph node (mLN) by cDC1s, driving the proliferation of antigen-specific CD4⁺ TCR-M T cells and their differentiation into regulatory

SUBMITTER: Van der Borght K 

PROVIDER: S-EPMC5379012 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature