Document Type
Article
Publication Date
2003
Publication Title
Proceedings of the National Academy of Sciences of the United States of America
Department
Geisel School of Medicine
Abstract
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.
DOI
10.1073/pnas.2131686100
Original Citation
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.
https://digitalcommons.dartmouth.edu/facoa/1473
