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The Journal of Immunology, 2004, 172: 195-201.
Copyright © 2004 by The American Association of Immunologists

Cognate B Cell Signaling via MHC Class II: Differential Regulation of B Cell Antigen Receptor and MHC Class II/Ig-{alpha}{beta} Signaling by CD221

David M. Mills, John C. Stolpa and John C. Cambier2

Integrated Department of Immunology, University of Colorado Health Sciences Center and National Jewish Medical and Research Center, Denver, CO 80206

Recent studies demonstrate that MHC class II molecules can signal via associated Ig-{alpha}{beta} dimers, signal transducers previously thought to function only in B cell Ag receptor (BCR) signaling. Surprisingly, the biologic outputs of MHC class II and BCR ligation (by thymus-dependent Ags) differ, e.g., MHC class II signaling leads to robust proliferation and extension of pseudopods. It seemed possible that these differences might be due, at least in part, to differential use of inhibitory coreceptors thought to modulate membrane Ig signals. In this study, we demonstrate that CD22, an inhibitory BCR coreceptor, neither associates with nor functions in MHC class II/Ig-{alpha}{beta} signaling. Interestingly, CD22 is actively excluded from cell surface MHC class II aggregates.




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