Burbage, MarianneKeppler, Selina J.Montaner, BeatrizMattila, Pieta K.Batista, Facundo2017-11-212017Burbage, Marianne, Selina J. Keppler, Beatriz Montaner, Pieta K. Mattila, and Facundo D. Batista. 2017. “The Small Rho GTPase TC10 Modulates B Cell Immune Responses.” The Journal of Immunology Author Choice 199 (5): 1682-1695. doi:10.4049/jimmunol.1602167. http://dx.doi.org/10.4049/jimmunol.1602167.http://nrs.harvard.edu/urn-3:HUL.InstRepos:34375111Rho family GTPases regulate diverse cellular events, such as cell motility, polarity, and vesicle traffic. Although a wealth of data exists on the canonical Rho GTPases RhoA, Rac1, and Cdc42, several other family members remain poorly studied. In B cells, we recently demonstrated a critical role for Cdc42 in plasma cell differentiation. In this study, we focus on a close homolog of Cdc42, TC10 (also known as RhoQ), and investigate its physiological role in B cells. By generating a TC10-deficient mouse model, we show that despite reduced total B cell numbers, B cell development in these mice occurs normally through distinct developmental stages. Upon immunization, IgM levels were reduced and, upon viral infection, germinal center responses were defective in TC10-deficient mice. BCR signaling was mildly affected, whereas cell migration remained normal in TC10-deficient B cells. Furthermore, by generating a TC10/Cdc42 double knockout mouse model, we found that TC10 can compensate for the lack of Cdc42 in TLR-induced cell activation and proliferation, so the two proteins play partly redundant roles. Taken together, by combining in vivo and in vitro analysis using TC10-deficient mice, we define the poorly studied Rho GTPase TC10 as an immunomodulatory molecule playing a role in physiological B cell responses.en-USJournal Article2017-11-2110.4049/jimmunol.1602167