| First Author | Voigt I | Year | 2000 |
| Journal | Eur J Immunol | Volume | 30 |
| Issue | 2 | Pages | 560-7 |
| PubMed ID | 10671212 | Mgi Jnum | J:60376 |
| Mgi Id | MGI:1353222 | Doi | 10.1002/1521-4141(200002)30:2<560::AID-IMMU560>3.0.CO;2-T |
| Citation | Voigt I, et al. (2000) CXCR5-deficient mice develop functional germinal centers in the splenic T cell zone. Eur J Immunol 30(2):560-7 |
| abstractText | The chemokine receptor CXCR5 is thought to be essential for the migration of B cells into the network of follicular dendritic cells in the spleen. However, as shown here, B cells and follicular dendritic cells do co-localize, albeit aberrantly, even in the absence of CXCR5. In mice lacking CXCR5 both cell types are found in a broad ring around the sinuses of the marginal zones. Upon immunization with the T cell-dependent antigen 2-phenyl-oxazolone, ectopic germinal centers develop in the periarteriolar lymphocyte sheath. A network of follicular dendritic cells forms in the vicinity of the central arteriole within which the antigen-activated B cells proliferate. The analysis of the expressed V gene repertoire revealed that during B cell proliferation, hypermutation is activated and V region genes accumulate somatic mutations. The pattern of somatic mutations suggests that affinity selection may occur. This analysis confirms that in CXCR5-deficient mice, the organization of splenic primary follicles is severely impaired. However, within the T cell zone a micro-environment is built up, which provides all requirements needed for the affinity maturation to take place. |
