Proceedings of the National Academy of Sciences of the United States of America
Geisel School of Medicine
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.
Erickson LD, Lin LL, Duan B, Morel L, Noelle RJ. A genetic lesion that arrests plasma cell homing to the bone marrow. Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12905-10. doi: 10.1073/pnas.2131686100. Epub 2003 Oct 10. PMID: 14555759; PMCID: PMC240717.
Dartmouth Digital Commons Citation
Erickson, Loren D.; Lin, Ling-Li; Duan, Biyan; Morel, Laurence; and Noelle, Randolph J., "A Genetic Lesion that Arrests Plasma Cell Homing to the Bone Marrow" (2003). Dartmouth Scholarship. 1473.