TCR-Induced Transmembrane Signaling by Peptide/MHC Class II Via Associated Ig-α/β Dimers

Author:

Lang Paul1,Stolpa John C.1,Freiberg Benjamin A.1,Crawford Frances2,Kappler John2,Kupfer Abraham1,Cambier John C.1

Affiliation:

1. Integrated Department of Immunology, University of Colorado Health Sciences Center, and National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206, USA.

2. Howard Hughes Medical Institute, National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206, USA.

Abstract

Previous findings suggest that during cognate T cell–B cell interactions, major histocompatability complex (MHC) class II molecules transduce signals, leading to Src-family kinase activation, Ca 2+ mobilization, and proliferation. Here, we show that antigen stimulation of resting B cells induces MHC class II molecules to associate with Immunoglobulin (Ig)-α/Ig-β (CD79a/CD79b) heterodimers, which function as signal transducers upon MHC class II aggregation by the T cell receptor (TCR). The B cell receptor (BCR) and MHC class II/Ig-α/Ig-β are distinct complexes, yet class II–associated Ig-α/β appears to be derived from BCR. Hence, Ig-α/β are used in a sequential fashion for transduction of antigen and cognate T cell help signals.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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