| First Author | Erickson LD | Year | 2003 |
| Journal | Proc Natl Acad Sci U S A | Volume | 100 |
| Issue | 22 | Pages | 12905-10 |
| PubMed ID | 14555759 | Mgi Jnum | J:99737 |
| Mgi Id | MGI:3583519 | Doi | 10.1073/pnas.2131686100 |
| Citation | Erickson LD, et al. (2003) A genetic lesion that arrests plasma cell homing to the bone marrow. Proc Natl Acad Sci U S A 100(22):12905-10 |
| abstractText | The coordinated regulation of chemokine responsiveness plays a critical role in the development of humoral immunity. After antigen challenge and B cell activation, the emerging plasma cells (PCs) undergo CXCL12-induced chemotaxis to the bone marrow, where they produce Ab and persist. Here we show that PCs, but not B cells or T cells from lupus-prone NZM mice, are deficient in CXCL12-induced migration. PC unresponsiveness to CXCL12 results in a marked accumulation of PCs in the spleen of mice, and a concordant decrease in bone marrow PCs. Unlike normal mice, in NZM mice, a majority of the splenic PCs are long-lived. This deficiency is a consequence of the genetic interactions of multiple systemic lupus erythematosus susceptibility loci. |
