International Immunology Advance Access originally published online on June 1, 2006
International Immunology 2006 18(7):1171-1178; doi:10.1093/intimm/dxl051
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CD21 and CD62L shedding are both inducible via P2X7Rs
1 Department of Biology, Immunology, Faculty of Sciences, University of Konstanz, D-78457 Konstanz, Germany
2 Biotechnology Institute Thurgau, Konstanzer Strasse 19, CH-8274 Tägerwilen, Switzerland
Correspondence to: H. Illges; E-mail: harald.illges{at}bitg.ch
Neutrophils and lymphocytes are recruited to sites of inflammation and require the adhesion molecule L-selectin (CD62L) for adherence to endothelial cells. Nucleotides released from activated or dying cells at sites of inflammation can mediate signaling through purinergic receptor family II, resulting in CD62L shedding. Activation of B lymphocytes requires the complement receptor type II (CD21) and at the same time leads to shedding of CD21. Both CD62L and CD21 shedding possibly depends on the same families of proteases. In the present study, we characterized peripheral blood naive and memory cells and neutrophils for CD62L surface expression and analyzed benzoyl-benzoyl triphosphate (BzATP)-induced shedding. BzATP is able to induce CD62L shedding in naive and memory lymphocytes, but not in neutrophils. CD21 shedding can be induced through activation of the B cell receptor (BCR) or with mitogens. Here we show that CD21 is also susceptible to BzATP-induced shedding on peripheral B cells. In addition, using receptor inhibitiors, we show that shedding of CD21 and CD62L is mediated via the P2X7R. P2X7R-mediated CD62L and CD21 shedding could occur as a result of extracellular accumulated ATP and may have an influence on leukocyte migrational behavior and BCR-mediated signaling.
Keywords: CD62L, CD21, ectodomain shedding, purinergic receptors, KN62, oxATP