Link to Pubmed [PMID] – 6234221
Immunol. Rev. 1984 Apr;78:211-24
T cell-dependent induction of small, resting B lymphocytes requires direct recognition of antigen and/or I-A/E molecules on the B cell surface by the inducing helper cell, and it does not require the participation of Ig receptors on the responding B cell. Triggering B cell receptors, therefore, are either the I-A/E molecules themselves, or other structures with complementarities on helper cell membranes that become available for productive interactions upon I-A/E recognition. It would appear that signal delivery by such triggering receptors can be regulated by a membrane complex of molecules, involving immunoglobulins, Class II MHC molecules and other classes of receptors, which in selective and distinct manners control the quantitative levels of expression and/or availability of the relevant structures. Classical in vivo observations and our in vitro experiments led us to conclude that induction of B cells does not occur upon binding of T cell-dependent antigens to Ig receptors and, consequently, that B lymphocyte activation by anti-receptor antibodies has no physiological counterpart. Induced B lymphocytes proliferate and mature to high rate secretion of antibodies under the influence of selective growth and maturation factors produced by helper cells which are MHC-unrelated, act polyclonally and have no influence in normal, resting cells. Specific ligand interactions with the membrane molecules participating of that functional complex may also regulate reactivity to either growth or maturation factors, and, thus, control clonal performances and the fate of activated cells.