| First Author | Han SB | Year | 2005 |
| Journal | Immunity | Volume | 22 |
| Issue | 3 | Pages | 343-54 |
| PubMed ID | 15780991 | Mgi Jnum | J:97001 |
| Mgi Id | MGI:3574135 | Doi | 10.1016/j.immuni.2005.01.017 |
| Citation | Han SB, et al. (2005) Rgs1 and Gnai2 Regulate the Entrance of B Lymphocytes into Lymph Nodes and B Cell Motility within Lymph Node Follicles. Immunity 22(3):343-54 |
| abstractText | Signaling by G protein-coupled receptors coupled to Galpha(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 Galpha(i1) and Galpha(i3) poorly compensate for the loss of Galpha(i2). These results demonstrate opposing roles for Rgs1 and Gnai2 in B cell trafficking into and within lymph nodes. |
