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Center point
Center pointCXCR4 desensitization inhibits the B cell cycle and differentiation after TLR activation
CXCR4 desensitization inhibits the B cell cycle and differentiation after TLR activationCXCR4 desensitization limits the intensity and duration of the immune response outside the follicle
CXCR4 desensitization limits the extrafollicular immune strength and duration of the reaction of the immuneThe extra-follicular immune response is essential for the production of a rapid transient wave of protective antibodies during infection
infection
In this study, Felix et al.
Cxcr4 the signaling receptor desensitization defects due to result in increased reinforcing outer follicular B cell response, and desensitization Cxcr4 limit cycle and generate B cells into plasma cells Cxcr4 signaling receptor desensitization due to a defect enhancement will Intensify the response of B cells outside the follicle, and Cxcr4 desensitization can restrict B cells from entering the circulation and the production of plasma cells
Cxcr4 desensitization restricts B cells from entering the circulation
Cxcr4 desensitization restricts B cells from entering the circulationUsing mouse models with gain-of-function mutations in Cxcr4 that are found in 2 human blood diseases, warts, hypogammaglobulinemia, infection and myelodysplastic syndrome (WHIM) and Waldenstrom macroglobulinemia, the researchers proved that, Compared with wild-type B cells, after Toll-like receptor (TLR) stimulation, mutant B cells exhibit enhanced rapamycin signaling mechanism targets, circulate more, and differentiate into plasma cells more efficiently
Compared with wild-type B cells, after Toll-like receptor (TLR) stimulation, mutant B cells exhibit enhanced rapamycin signaling mechanism targets, circulate more, and differentiate into plasma cells more efficiently
Cxcr4 desensitization restricts plasma cell differentiation
Cxcr4 desensitization restricts plasma cell differentiationIn addition, the gain-of-function mutation of Cxcr4 also promoted the homing and persistence of immature plasma cells in the bone marrow, which was reproduced in samples of patients with WHIM syndrome
In summary, the results of this study indicate that Cxcr4 desensitization plays a key role in the process of B cell activation and plasma cell differentiation, and fine-tuning of Cxcr4 signal is essential to limit the intensity and duration of the immune response outside the follicle
Cxcr4 desensitization plays a key role in the process of B cell activation and plasma cell differentiation.
Original source:
Alouche Nagham,Bonaud Amélie, Rondeau Vincent et al.
Hematologic disorder-associated Cxcr4 gain-of -function mutation leads to uncontrolled extrafollicular immune response
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