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- W2980636260 abstract "RasGRP1 is a key molecule that mediates antigen-initiated signaling for activation of the RAS-MAPK pathway in lymphocytes. Patients with aberrant RasGRP1 expression experience lymphocyte dysfunction and are afflicted with recurrent microbial infections. Yet, the underlying mechanism that accounts for microbial infection remains unknown. We previously reported that B1a cells are heterogeneous with respect to PD-L2 expression and that RasGRP1 deficiency preferentially impairs PD-L2+ B1a cell development. In the present study, we show that PD-L2+ B1a cells exhibit increased capacity for differentiation to CD138+ plasma cells that secrete natural IgM antibody, as well as IL-10 and GM-CSF, in response to TLR stimulation. In keeping with this, we show here that RasGRP1-deficent mice are much more susceptible to septic infection triggered by cecal ligation and puncture than wild type mice, and that reconstitution of RasGRP1-deficient mice with wild type PD-L2+ B1a cells greatly rescues RasGRP1-deficient mice from sepsis. Thus, this study indicates a mechanism for the association of RasGRP1 deficiency with predispostion to infection in the loss of a particular B1a subpopulation." @default.
- W2980636260 created "2019-10-25" @default.
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- W2980636260 date "2019-12-01" @default.
- W2980636260 modified "2023-09-26" @default.
- W2980636260 title "Impairment of PD-L2 positive B1a cells enhances susceptibility to sepsis in RasGRP1-deficient mice" @default.
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- W2980636260 doi "https://doi.org/10.1016/j.cellimm.2019.103993" @default.
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