Receptor editing in CD45‐deficient immature B cells

B cell receptor signaling threshold regulates negative selection of autoreactive B cells and determines the mechanism of B cell tolerance. Using mice carrying immunoglobulin transgene specificfor MHC class I antigen Kk (3–83Tg mice), and IL‐7‐driven bone marrow (BM) culture system, we have previously shown that receptor editing is a major mechanism in B cell tolerance. To test the role of BCR signaling competence on the induction of tolerance‐mediated receptor editing, we crossed the 3–83Tg mice with mice deficient in CD45, a protein tyrosine phosphatase that functions asa positive regulator of the BCR signaling. We found that in the absence of self‐antigen allelic exclusion is efficiently imposed in 3–83Tg CD45–/– mice, although numbers of peripheral B cells are reduced. Using our BM culture system, we show here that immature 3–83Tg CD45–/– B cells encountering self‐antigen are developmentally arrested and undergo secondary light chain recombination and receptor editing, not different than CD45‐sufficient cells. Thus, lack of CD45 does not abolish the receptor editing competence in immature B cells encountering high avidity membrane‐bound antigen.