Abstract

It is clear that anti-CD3-activated T cells provide all the signals necessary for polyclonal activation, proliferation and differentiation of human B cells. B-cell activation, proliferation and differentiation are initiated by a complex series of receptor-ligand interactions, of which LFA-1-ICAM-1 ligation plays a central, but not exclusive role. In addition, the action of a number of cytokines, most prominently IL2, is essential for B-cell proliferation and differentiation. It is apparent from the results obtained using this model system that the conjugate formation that occurs as part of antigen presentation and T-cell activation is not required for the subsequent collaboration between activated T cells and B cells necessary to trigger B-cell responses. The implication of these studies is that after initial antigen recognition and T-cell activation, T cell/B cell collaboration leading to antibody production is antigen non-specific and potentially capable of inducing polyclonal B-cell responses. Conjugate formation that develops as part of antigen presentation may tend to focus the response and limit the B cells that can be induced to respond. Alternatively, T-cell recognition of antigen may deliver a signal to the B cell by cross-linking MHC molecules bearing the recognized antigenic fragment that makes it more capable of responding to the T-cell-derived antigen-non-specific signals and cytokines promoting B-cell activation, proliferation and differentiation.

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