By M. Eric Gershwin, Richard S. Beach, Lucille S. Hurley
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Example text
These studies taken together strongly suggested the existence of thymic regulation by suppression of the antibody response to several antigens requiring little thymic helper function. In addition, suppression has been demonstrated for antigens requiring thymic helper cells for a maximum antibody response. Similarly, the homocytotrophic (IgE) antibody response to dinitrophenyl-ascaris may be regulated by antigen-specific suppression. In cell-mediated systems, suppression of the induction of graftversus-host disease by thymocytes and spleen cells has been demonstrated.
Similarly, a select population of B cells does not produce antibody but nevertheless differentiates and survives for long periods of time as memory cells. These latter cells are capable of responding after secondary challenge or exposure to antigen and therefore produce the anamnestic response. In contrast to humoral immunity, cell-mediated immunity is directly under the influence of thymic-derived T cells. The mechanism by which T cells recognize antigens and produce positive signals, in contrast to the above information on B cells, is unclear.
The mechanism of suppression is poorly understood. Preliminary results suggest that in the antibody systems thymic suppression may act by inhibiting B-cell proliferation. A similar suppression of T-cell proliferation would be plausible for the cellular system, including graft-versus-host disease. In the normal host, however, there is probably a balance between suppressor and proliferative functions. Chronic allogeneic disease may be an example of relative reduction in suppressor function secondary to a pronounced enhancement of proliferative function.
