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International Immunology, Vol. 14, No. 2, 139-146, February 2002
© 2002 Japanese Society for Immunology

Depletion of Lyn kinase from the BCR complex and inhibition of B cell activation by excess CD21 ligation

Leena Chakravarty, Mark D. Zabel, Janis J. Weis and John H. Weis

Division of Cell Biology and Immunology, Department of Pathology, University of Utah, School of Medicine, 50 N. Medical Drive, Salt Lake City, UT 84132, USA

Correspondence to: J. H. Weis; E-mail: john.weis{at}path.utah.edu

The human and murine CD21 gene products have been functionally linked to B cell activation by the co-ligation of the BCR and the CD21/CD19/CD81 complexes. Binding of low levels of antigen complexed to the complement ligand(s) for CD21 enhances B cell activation compared to the stimulation caused by antigen alone. Mice lacking functional CD21 predispose to autoimmune responses suggesting that this receptor may also play a negative role: thus in the presence of excess complement-bearing immune complexes, B cell antigen-specific activation may be inhibited. This possibility was investigated using intracellular calcium elicitation analyses to follow BCR-mediated activation. Ligation of the BCR and limiting quantities of the CD21 receptor demonstrated the expected enhanced cellular response compared to BCR ligation alone: CD21 ligation alone demonstrated no alteration in calcium flux. However, co-ligation of the BCR with excess CD21 binding resulted in the elimination of the calcium response, suggesting that CD21 ligation was down-modulating the BCR response. Immunoprecipitation of kinases associated with the BCR and CD21/CD19/CD81 complexes demonstrated that Lyn is preferentially depleted from the BCR complex following excess binding of CD21. Localization of other kinases integral for B cell activation is not altered. These data suggest that excess CD21 ligand binding can negatively impact B cell activation by sequestering Lyn kinase away from the BCR complex.

Keywords: B cells, cellular activation, CD21, complement, Lyn

Transmitting editor: T. F. Tedder


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