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

Loren D. Erickson, Ling Li Lin, Biyan Duan, Laurence Morel, Randolph J. Noelle

Research output: Contribution to journalArticlepeer-review

58 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)12905-12910
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume100
Issue number22
DOIs
StatePublished - Oct 28 2003
Externally publishedYes

ASJC Scopus subject areas

  • General

Fingerprint

Dive into the research topics of 'A genetic lesion that arrests plasma cell homing to the bone marrow'. Together they form a unique fingerprint.

Cite this