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- W4313385060 abstract "Abstract Mer receptor tyrosine kinase (Mer) signaling maintains immune tolerance by clearing apoptotic cells and inducing immunoregulatory signaling cascades. We previously showed that Mer-deficient mice on a mixed B6 and 129 background (B6129F2.Mer−/−) have increased germinal center (GC) responses, T cell activation, and apoptotic cell accumulation within GCs. Whereas B6129F2.Mer−/− mice accumulate apoptotic cells in GCs, B6.Mer−/− mice do not accumulate apoptotic cells, resembling B6 mice. Therefore, we used these two models to mechanistically separate the effects of debris released from secondary necrotic cells as a result of apoptotic cell accumulation from those driven by the loss of immune regulation by Mer. Through the study of global and cell-type intrinsic TLR and MyD88 deficiency in B6129F2.Mer−/− mice, we found that GC B cell-intrinsic sensing of self-RNA, but not self-DNA, released from secondary necrotic cells drives self-antigen induced GC responses. While self-ligands drive the magnitude of GC response, the loss of Mer immunoregulatory signaling bolsters antigen presentation and APC-intrinsic TLR activation drives pro-inflammatory cytokine production. Further, the loss of Mer immunoregulatory signaling accelerates the onset of autoimmunity when B6.Mer−/− mice are crossed to autoimmune-prone B6.Sle1b mice (Sle1b.Mer−/−) due to the retention of autoreactive B cells in GCs. Collectively, Mer prevents the cell-intrinsic activation of GC B cells and APCs to regulate the magnitude of GC response and T cell activation, in addition to regulating GC selection events to prevent the development of autoimmunity." @default.
- W4313385060 created "2023-01-06" @default.
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- W4313385060 date "2017-05-01" @default.
- W4313385060 modified "2023-09-27" @default.
- W4313385060 title "Mer receptor tyrosine kinase signaling prevents TLR-mediated self-ligand sensing and aberrant selection in germinal centers" @default.
- W4313385060 doi "https://doi.org/10.4049/jimmunol.198.supp.207.1" @default.
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