Effector memory CD4+ T cells induce damaging innate inflammation and autoimmune pathology by engaging CD40 and TNFR on myeloid cells

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Effector memory CD4+ T cells induce damaging innate inflammation and autoimmune pathology by engaging CD40 and TNFR on myeloid cells
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A new SciImmunology study in mice shows how blocking interaction between effector memory T cells and myeloid cells can prevent innate inflammation contributing to autoimmune diseases.

Whereas autoreactive T cells are believed to be key drivers of pathology in many autoimmune diseases, myeloid cells are major producers of proinflammatory cytokines that can further exacerbate tissue damage. McDanieldemonstrate that innate inflammation in mice can be initiated by effector memory T cells , and this sterile inflammatory program closely resembles the response to microbial recognition.

Although blocking individual cytokines can mitigate some pathology, the upstream mechanisms governing overabundant innate inflammatory cytokine production remain unknown. Here, we have identified a critical signaling node that is engaged by effector memory T cells to mobilize a broad proinflammatory program in the innate immune system.

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