| First Author | Moratz C | Year | 2004 |
| Journal | Mol Cell Biol | Volume | 24 |
| Issue | 13 | Pages | 5767-75 |
| PubMed ID | 15199133 | Mgi Jnum | J:90780 |
| Mgi Id | MGI:3044745 | Doi | 10.1128/MCB.24.13.5767-5775.2004 |
| Citation | Moratz C, et al. (2004) Abnormal B-cell responses to chemokines, disturbed plasma cell localization, and distorted immune tissue architecture in Rgs1-/- mice. Mol Cell Biol 24(13):5767-75 |
| abstractText | Normal lymphoid tissue development and function depend upon chemokine-directed cell migration. Since chemokines signal through heterotrimeric G-protein-coupled receptors, RGS proteins, which act as GTPase-activating proteins for Galpha subunits, likely fine tune the cellular responses to chemokines. Here we show that Rgs1(-/-) mice possess B cells that respond excessively and desensitize improperly to the chemokines CXCL12 and CXCL13. Many of the B-cell follicles in the spleens of Rgs1(-/-) mice have germinal centers even in the absence of immune stimulation. Furthermore, immunization of these mice leads to exaggerated germinal center formation; partial disruption of the normal architecture of the spleen and Peyer's patches; and abnormal trafficking of immunoglobulin-secreting cells. These results reveal the importance of a regulatory mechanism that limits and desensitizes chemokine receptor signaling. |
