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Integrated Department of Immunology, University of Colorado School of Medicine and National Jewish Medical and Research Center, Denver, CO 80206
Resting B lymphocytes have been credited with inducing T cell
tolerance to Ig-derived and monovalent self-Ags that are internalized
via the B cell receptor (BCR). These conclusions are predicated upon
the assumptions that resting B cells display BCR-associated peptides in
class II MHC and that the cells remain quiescent during the course of
experimental manipulation. To determine whether resting B cells display
BCR-associated epitopes in class II MHC, we devised a sensitive assay
that averted potential activation of B cells by Ag and minimized
activation by prolonged culture. Ex vivo, Percoll-fractionated B cells
expressing a 
transgene encoding a T cell epitope were cultured with
a reactive T cell hybridoma for 12 h. Whereas low density,
LPS-activated, and BCR-activated B cells elicited significant IL-2 from
the T cell hybridoma, resting high density B cells did not. Parallel
results were obtained with normal B cells expressing a second epitope
encoded by an endogenous VH gene. Anergic B cells, which
are uniformly low density, also significantly stimulated the T cell
hybridoma. Finally, longer culture periods with normal B cells resulted
in a higher degree of B cell activation and significant stimulation of
reactive T cell hybridomas. Our results provide evidence that
activation of B cells profoundly enhances the processing and
presentation of BCR-associated Ags.
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