The T-lymphocyte population is divisible into several subclasses; each subclass possesses a distinctive genetic program which combines information for cell-surface phenotype and function (1). In the mouse, there is evidence that T cells which express the Thyl+Lyl+Ly23 -surface phenotype CLyl cells") are programmed for helper (TH) 1 function. In contrast, T cells that express the Thyl+Lyl-Ly23 ÷ surface phenotype CLy23 cells") are programmed for suppressor (Ts) function (1). Isolation of these two T-cell subclasses in mice depleted of T cells CB mice") has indicated that each belongs to an independent line or branch of thymus-dependent differentiation (2). A third major T-cell subclass, expressing the surface phenotype Lyl+2+3 +, can react to antigen and differentiate to Ly23 + cytotoxic effector cells (3), suggesting that this subclass probably contains precursor cells that have acquired receptors for antigen but have not yet become committed to either TH or Tc~s function (3).These findings, and others, are consistent with the view that functionally distinct T-cell sets carry cell surface components that are invariably associated with particular immunologic function. According to this idea, cells carrying the Lyl+Ly23 -surface phenotype are programmed for helper and not suppressive activity regardless of external conditions, such as the mode or type of antigen stimulation. To test this hypothesis we have stimulated purified populations of Lyl+2 -T cells with antigen in vitro, by using conditions devised to induce unselected T cells to express optimal levels of antigen-specific suppressive activity (4). We find that (a) stimulation of purified Lyl cells under these conditions results in the generation of TH but not Ts activity and (b) such hyperimmune Lyl cells also induce a subset of nonimmune T cells to exert potent suppressive effects upon the antibody response. The surface phenotype of the T-cell set responsible for "feedback" inhibition is described in this study.
Alginic acid-like mucoid exopolysaccharide was isolated from three strains of Pseudomonas aeruginosa obtained from the sputa of patients with cystic fibrosis. Purified mucoid antigens were greater than 99% uronic acid. With a hemagglutination assay, antibody responses to the mucoid exopolysaccharide were documented after immunization of rabbits with either whole mucoid organisms or purified mucoid exopolysaccharide. The mucoid antigen from one strain (no. 2192) was composed predominantly of a single serologic epitope shared among 40 alginate exopolysaccharides from different clinical isolates. The mucoid exopolysaccharide from the other two strains (nos. 1 and 258) had a serotype-specific determinant in addition to the common epitope. Analyses of antibody in sera from normal adults, children, and patients with cystic fibrosis culture-positive and culture-negative for mucoid P. aeruginosa showed a highly significant (P less than 0.001) association between increased hemagglutination titers and positive cultures for mucoid P. aeruginosa.
Strains of Staphylococcus aureus isolated from patients with toxic shock syndrome (TSS) make a characteristic protein known as toxic-shock-syndrome toxin-1 (TSST-1), but the role of this protein in the pathogenesis of TSS is not certain. We have purified TSST-1 by using a combination of alcohol precipitation, isoelectric focusing, and gel chromatography. TSST-1 has an isoelectric point of 7.2 and a molecular weight of 23,100, in accordance with previously published determinations for this protein, and is serologically identical to pyrogenic exotoxin C and staphylococcal enterotoxin F. In highly purified form, TSST-1 is a potent inducer of interleukin-1 production by human monocytes, as quantitated in a thymocyte-proliferation assay. This capability is not attributable to contamination by other staphylococcal products or gram-negative endotoxin and can be blocked by hydrocortisone. Many features of TSS suggest that induction of interleukin-1 by TSST-1 in vivo may play a central role in the elaboration of this disease.
We have described an interaction between two T cells subsets that results in interference with the expression of Ly-1-, 2+ (Ly-2) T cell-mediated suppression. We refer to this novel immunoregulatory activity as contrasuppression. The T cell responsible for the induction of contrasuppression (inducer cell) expresses the phenotype Ly-1-, 2+;I-J+;Qa-1+. This phenotype distinguishes it from the suppressor effector cells which we find to be I-J-2.3. An I-J+ soluble mediator from the contrasuppressor inducer cell acts on another cell (acceptor cell) that expresses the phenotype Ly-1+, 2+; I-J+; Qa-1+. This phenotype distinguishes it from T helper cells. Both the inducer cell (or its biologically active mediator) and its acceptor cell are required for the expression of contrasuppression. Because contrasuppressor cells can block the suppressive activity of cell-free mediators released by Ly-2 suppressor T cells, the mechanism of contrasuppression is either separated from or in addition to the inactivation of suppressor cells themselves. The potential importance of contrasuppressor activity in the regulation of suppressor T cell activity in allowing immunologic memory to be expressed and in permitting microenvironmental immune regulation is discussed.
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