Journal
CURRENT OPINION IN IMMUNOLOGY
Volume 18, Issue 2, Pages 184-190Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2006.01.005
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Funding
- NIAID NIH HHS [R01 AI052310, R21 AI063321, R01 AI052157] Funding Source: Medline
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Receptor editing has emerged from its original identification as a minor secondary mechanism of B cell tolerance to be considered as a dominant mechanism by which autoreactive immature B cells are rendered tolerant. Clonal deletion, previously regarded as the major mechanism of central B cell tolerance, has been shown by recent studies to operate secondarily and only when receptor editing is unable to provide a non-autoreactive specificity. Receptor editing has also been shown to operate during the development of wild-type B lymphocytes, and ongoing investigations demonstrate the influence of particular signaling molecules in the induction and/or inhibition of receptor editing. Together, these studies begin to map the signaling pathways that regulate receptor editing in autoreactive and non-autoreactive immature B cells.
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