Rgs1 and Gnai2 regulate the entrance of B lymphocytes into lymph nodes and B cell motility within lymph node follicles

Signaling by G protein-coupled receptors coupled to G alpha(i) assists in triggering lymphocyte movement into and out of lymph nodes. Here, we show that modulating the signaling output from these receptors dramatically alters B cell trafficking. Intravital microscopy of adoptively transferred B cells from wild-type and Rgs1(-/-) mice revealed that Rgs1(-/-) B cells stick better to lymph node high endothelial venules, home better to lymph nodes, and move more rapidly within lymph node follicles than do wild-type B cells. In contrast, B cells from Gnai2(-/-) mice enter lymph nodes poorly and move more slowly than do wild-type B cells. The Gnai2(-/-) mice often lack multiple peripheral lymph nodes, and their B cells respond poorly to chemokines, indicating that G alpha(i1) and G alpha(i3) poorly compensate for the loss of G alpha(i2). These results demonstrate opposing roles for Rgs1 and Gnai2 in B cell trafficking into and within lymph nodes.