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Arhgap25 deficiency leads to decreased numbers of peripheral blood B cells and defective germinal center reactions

By Silke E. Lindner, Colt A. Egelston, Stephanie M. Huard, Peter P Lee, Leo D. Wang

Posted 06 Mar 2020
bioRxiv DOI: 10.1101/2020.03.05.965228 (published DOI: 10.4049/immunohorizons.2000021)

Rho family GTPases are critical for normal B cell development and function and their activity is regulated by a large and complex network of guanine nucleotide exchange factors (GEFs) and GTPase activating proteins (GAPs). However, the role of GAPs in B cell development is poorly understood. Here we show that the novel Rac-GAP ARHGAP25 is important for B cell development in a CXCR4-dependent manner. We show that Arhgap25 deficiency leads to a significant decrease in peripheral blood B cell numbers, as well as defects in mature B cell differentiation. Arhgap25-/- B cells respond to antigen stimulation in vitro and in vivo but have impaired germinal center formation and decreased IgG1 class switching. Additionally, Arhgap25-/- B cells exhibit increased chemotaxis to CXCL12. Taken together, these studies demonstrate an important role for Arhgap25 in peripheral B cell development and antigen response.

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