Contrasuppression: the second law of thymodynamics, revisited.
The data discussed here touch upon several issues in the evolving story of T cell contrasuppression, the underlying theme being that of heterogeneity. First, there is the issue of function. We are considering here only those cells that affect the function of secretory differentiation. We have evidence that different contrasuppressor cells exist for clone growth, but have not yet studied them in the same depth as those for secretory differentiation. Second, there is the important issue of target cells. In this article by Green and Gershon it is pointed out that there is clear evidence that contrasuppressor effects can work by protecting helper cells from suppressor cell effects in vitro. On the other hand, direct additional inhibition of the suppressor cells themselves has not been excluded. The latter point is also true in our system. However, we must suppose for the sake of simplicity in many of our experiments that if suppressors are not the target of the contrasuppressor effects then the B cells themselves probably are. This is because the tumor cells engage in a spontaneous rate of growth and differentiation in the absence of help or suppression. When T cell-dependent, specifically triggered effects reduce this spontaneous behavior, then a suppressive effect must have been delivered directly to the B cells. This is a simplifying assumption which is attractive, but since the experiments are carried out in vivo and thus may be affected by some factors that we have not yet recognized, we are not confident on its "intuitive" appeal. A third issue revolves around triggering specificity. One of our contrasuppressors exhibits the phenomenon of carrier crossreactivity (CRCS) and is thus behaving in accord with expectations aroused by Green and Gershon in this review. The other cell is apparently quite carrier specific (SCS). The meaning of this is not at all clear, but its potential significance may somehow be related to a sort of "mirror image" relationship of the two cells. Thus, for example, in other experiments not discussed here, we have noted that the CRCS binds to 315 protein-coated plates, but as noted here counteracts a suppressive effect which is generated by cells which do not adhere to these plates. In contrast to SCS does not bind to 315 plates and yet, as noted here, appears to counteract a suppressor effect generated by cells which do adhere to 315 plates.(ABSTRACT TRUNCATED AT 400 WORDS)
D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology; D000954:Antigens, Surface / Q000032:analysis; D002478:Cells, Cultured; D000939:Epitopes / Q000032:analysis; D006087:Graft vs Host Reaction; D006801:Humans; D007108:Immune Tolerance; D007113:Immunity, Innate; D007116:Immunization, Passive; D007136:Immunoglobulins / Q000276:immunology; D008288:Malaria / Q000276:immunology; D051379:Mice; D008808:Mice, Inbred CBA; D009374:Neoplasms, Experimental / Q000235:genetics / Q000276:immunology*; D010641:Phenotype; D013154:Spleen / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D000954:Antigens, Surface; D000939:Epitopes; D007136:Immunoglobulins