期刊
JOURNAL OF CLINICAL IMMUNOLOGY
卷 28, 期 -, 页码 S42-S45出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10875-008-9182-7
关键词
common variable immune deficiency; memory B cell; pathogenesis; autoimmunity
类别
资金
- NIAID NIH HHS [P01 AI061093-05, P01 AI061093, P01 AI061093-04] Funding Source: Medline
Introduction About 20% of subjects with common variable immune deficiency (CVID) develop an autoinimune complication, most often immune thrombocytopenia or hemolytic anemia. While the pathogenesis of autoreactivity is unknown for CVID subjects in general, and to a greater extent in those with autoimmunity, there is a loss of switched memory B cells. Discussion About 7-8% of CVID subjects have mutations in the transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI), a significant association with this immune defect, although the same mutations may be found in normal relatives and rarely in healthy blood donors. In addition to generalized B cell dysfunction, defective elimination of autoimmune B cells has been demonstrated.
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