Abstract
I. Introduction. The system of the immune response to antigen is regulated by a series of interaction among B cells, T cells, and probably macrophages. Each B cell is genetically committed to become an antibody (immunoglobulin, 1g)-secreting cell against a distinct antigen epitope (l), and the antibody produced plays a key role in neutralizing relevant pathogenic microorganisms or in eliminating unnecessary molecules in the body.
It was shown that a T cell responding to, and specific for, the same antigen molecule was necessary for the B-cell response to that antigen (2-5). Two models were proposed to account for T-cell requirement for B-cell triggering: (a) that the T-cell help was delivered by a direct cell contact with B cells, and (b) that the T cell could produce a factor which acted, only at short range, on a receptor on the B-cell surface (6). There is now evidence that helper T cells recognize antigen in the context of class I1 major histocompatibility complex (MHC) molecules on accessory cells and/or B cells (7). It seems clear that the above two models represent two different mechanisms, and there is a consensus among many investigators that the direct Tcell- B-cell interaction is essential for the initial B-cell activation in the physiological environment of the whole animal. In the factor model, T cells can be activated by cell contact with B cells to produce an antigen nonspecific soluble factor in the vicinity of the B cell, and the B cell could respond in the absence of the T cell if a sufficient amount of the factor is provided. Actually, there is abundant evidence for a variety of T-celland macrophage-derived factors which act on B cells. These factors are non-antigen-specific, MHC unrestricted and are able to exert a variety of different functions.
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