An Overview of T-Suppressor Cell Circuits

Abstract

This review gives an overview of two main suppressor circuits. In its complete form, the first circuit form has an early acting Ts-inducer that behaves like a T-helper cell for the production of idiotype-directed Ts-transducer or antigen-directed Ts-effector cells. In this circuit, the T-suppressor effector cell (Ts-eff) produces antigen-specific T-suppressor factor (TsF). This has a mode of action through the T-acceptor cell (T-acc), a cell that requires immunization, but not specific immunization, for its production. This cell, when armed with TsF-eff and then triggered with antigen and I-J, releases nonspecific TsF that blocks the passive transfer of contact sensitivity. It also blocks the production of IL-2. The biological significance of the complexities of this circuit is discussed in relation to the control of unresponsiveness and the handling infection and antigenic variation of microorganisms. The second set of suppressor cells, T suppressor afferent cells, inhibits only when given early in the immune response but differs from the Ts-inducer by lacking an obligatory mode of action through the Ts-eff/T-acc circuit. In general, the antigen-specific T-helper and T-suppressor factors have a two-chain disulfide-bonded structure. One chain carries the antigen-binding site and the other chain MHC-related determinants. Both chains are required for biological activity, and the genetic restriction in this complementation implies that the antigen-binding chain has a recognition site for MHC determinant(s). The generalization can be made that the MHC-related determinants carried by the factors and the genetic restriction in their induction, in their action, and in the interchain complementation between their separated chains all map to the same region of the genome. This is intelligible on the assumption that the T-cell receptor on the cell that produces the factor has a recognition site for antigen and MHC determinants and that the antigen-binding chain of secreted factor has the same properties.

Depletion of OX-8 lymphocytes from the blood and airways using monoclonal antibodies enhances the late airway response in rats.

“…The sequence of events involved in immunosuppression is not entirely clear, but it has been postulated that Ts cells release suppressive factors that bind to antigen-presenting cells and other cells in secondary lymphoid tissue, and that these cells suppress effector cells such as T or B lymphocytes that arrive in that tissue (38,39). Inhibition ofTs using monoclonal antibodies could interfere with such mechanisms.…”

A single dose of UV radiation suppresses delayed type hypersensitivity responses to alloantigens and prolongs heart allograft survival in mice

“…CHS was determined as described by Asherson et ai (14). Mice were sensitized by application of 100 |il of a 1% (w/v) alcohol solution of oxazolone (OX) (4-ethoxy-methylene-2-phenyl oxazolone, Sigma Chemical Co., St Louis.…”

Production of suppressor factors induced by ultraviolet irradiation or cis‐urocanic acid requires Lyt‐2+ lymphocytes

“…Supernatants from these cultures contained soluble antigennon-specific SF, assayed by their ability to suppress antigen-stimulated SC proliferation. UVR-unrelated suppression in CHS involves several cells and factors (12). One such factor, produced by Cy-sensitive, Lyt-2 + cells is an antigen-non-specific SF (named nsTsF-1), capable of suppressing the adoptive transfer of CHS (20).…”

“…SF associated with immunosuppression in CHS and other immune phenomena are usually produced by T suppressor (Ts) lymphocytes, in a complex cascade of events (11,12). A simple way of investigating the role of T cell subsets in UVRinduced immunosuppression is to measure the effect of removing specific subsets by treatment with monoclonal antibodies (MoAb) directed against surface markers.…”