Abstract
Loss of lymphocytes, particularly Tcell apoptosis, is a central pathological event after severe tissue injury that is associated with increased susceptibility for life-threatening infections. The precise immunological mechanisms leading to Tcell death after acute injury are largely unknown. Here, we identified a monocyte-T cell interaction driving bystander cell death of Tcells in ischemic stroke and burn injury. Specifically, we found that stroke induced a FasL-expressing monocyte population, which led to extrinsic Tcell apoptosis. This phenomenon was driven by AIM2 inflammasome-dependent interleukin-1β (IL-1β) secretion after sensing cell-free DNA. Pharmacological inhibition of this pathway improved Tcell survival and reduced post-stroke bacterial infections. As such, this study describes inflammasome-dependent monocyte activation as a previously unstudied cause of Tcell death after injury and challenges the current paradigms of post-injury lymphopenia.
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