Cutting edge:: B-1 cells are deficient in Lck:: Defective B cell receptor signal transduction in B-1 cells occurs in the absence of elevated Lck expression

B-1 cells constitute a unique B cell subset that is primarily responsible for producing nonimmune Ig. This natural Ig acts as a principal line of defense against infection. A key feature of B-1 cells is the failure of BCR-triggered signal transduction. Recently, defective BCR signaling in B-1 cells bas been attributed to elevated expression of the canonical T cell src kinase, Lck. In the present study, we reexamined Lck expression in normal B-1 cells. We found that B-1 cells expressed less Lck at both the protein and RNA levels than did B-2 cells. The same B-1 cells manifested defective BCR-mediated induction of IKK beta phosphorylation, I kappa B alpha degradation, and intracellular Ca2+ mobilization. Thus, the failure of BCR signaling in B-1 cells does not relate to subset-specific elevation of Lck.