| First Author | Burbage M | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 5 | Pages | 1682-1695 |
| PubMed ID | 28747344 | Mgi Jnum | J:248522 |
| Mgi Id | MGI:6093993 | Doi | 10.4049/jimmunol.1602167 |
| Citation | Burbage M, et al. (2017) The Small Rho GTPase TC10 Modulates B Cell Immune Responses. J Immunol 199(5):1682-1695 |
| abstractText | Rho 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. |
