A genetic lesion that arrests plasma cell homing to the bone marrow
LD Erickson, LL Lin, B Duan… - Proceedings of the …, 2003 - National Acad Sciences
LD Erickson, LL Lin, B Duan, L Morel, RJ Noelle
Proceedings of the National Academy of Sciences, 2003•National Acad SciencesThe 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 …
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 …
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.
National Acad Sciences
