Recent advances in the understanding of the collaboration between T ce
lls and B cells have provided a novel framework within which to analys
e the mechanisms of B-cell tolerance and its breakdown. Of particular
interest has been the finding that B cell anergy is due to defective a
ntigen receptor mediated functions, while the antigen-processing machi
nery and CD40-dependent activation pathways are unaffected. Thus, the
anergic B cell, which otherwise has a short lifespan, can be rescued b
y a number of regimes to participate in autoimmune responses.