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The Rho GTPases Cdc42, Rac1, and Rac2 coordinate receptor signaling to cell adhesion, migration, and proliferation. Deletion of Rac1 and Rac2 early during B cell development leads to failure in B cell entry into the splenic white pulp. Here, we sought to understand the role of Rac1 and Rac2 in B cell functionality and during the humoral antibody response. To circumvent the migratory deficiency of B cells lacking both Rac1 and Rac2, we took the approach to inducibly delete Rac1 in Rac2 −/−  B cells in the spleen (Rac1 B Rac2 −/−  B cells). Rac1 B Rac2 −/−  mice had normal differentiation of splenic B cell populations, except for a reduction in marginal zone B cells. Rac1 B Rac2 −/−  B cells showed normal spreading response on antibody-coated layers, while both Rac2 −/−  and Rac1 B Rac2 −/−  B cells had reduced homotypic adhesion and decreased proliferative response when compared to wild-type B cells. Upon challenge with the T-cell-independent antigen TNP-conjugated lipopolysaccharide, Rac1 B Rac2 −/−  mice showed reduced antibody response. In contrast, in response to the T-cell-dependent antigen sheep red blood cells, Rac1 B Rac2 −/−  mice had increased serum titers of IgG1 and IgG2b. During  in vitro  Ig class switching, Rac1 B Rac2 −/−  B cells had elevated germline γ2b transcripts leading to increased Ig class switching to IgG2b. Our data suggest that Rac1 and Rac2 serve an important role in regulation of the B cell humoral immune response and in suppressing Ig class switching to IgG2b.

The Small Rho GTPases Rac1 and Rac2 Are Important for T-Cell Independent Antigen Responses and for Suppressing Switching to IgG2b in Mice