期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 100, 期 22, 页码 12905-12910出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.2131686100
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资金
- NCI NIH HHS [CA 23108, P30 CA023108] Funding Source: Medline
- NCRR NIH HHS [P20 RR016437, P20 RR 16437] Funding Source: Medline
- NIAID NIH HHS [R01 AI026296, R37 AI026296, AI 26296, AI 42234] Funding Source: Medline
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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