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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 Expression¹

Rubén Francés^*, Joseph R. Tumang and Thomas L. Rothstein^2,,

Departments of^* Medicine and Microbiology, Boston University School of Medicine, and Immunobiology Unit, Evans Memorial Department of Clinical Research, Boston University Medical Center, Boston, MA 02118

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 has been attributed to elevated expression of the canonical T cell src kinase, Lck. In the present study, we re-examined 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 phosphorylation, IB degradation, and intracellular Ca²⁺ mobilization. Thus, the failure of BCR signaling in B-1 cells does not relate to subset-specific elevation of Lck.

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