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Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12905-10. Epub 2003 Oct 10.

A genetic lesion that arrests plasma cell homing to the bone marrow.

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  • 1Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA.


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.

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