Conclusions
Since our long-term research interest is in immune-mediated interstitial renal disease, these are the models in which we have studied the role of contrasuppression in autoimmunity. Clearly, there is no a priori reason why this should be an immunopathogenic mechanism limited to T cell-mediated tubulointerstitial disease. Indeed, early support for this kind of mechanism was previously obtained in a model of systemic autoimmunity induced by polyclonal B cell activators [25]. There are other autoimmune diseases in which Ts cells have been implicated as tolerogenic mechanisms. These include experimental type I diabets (BB rats [26] and NOD mice [8]), thyroiditis [4], oophoritis [27], and experimental allergic encephalomyelitis [28]. Contrasuppression may well be operative, at least as one process in determining susceptibility to these organ-specific autoimmune lesions. It is important to note that since the effector and regulatory T cells may belong to the same phenotypic subset, identifying a T cell subset which ‘transfers disease’ does not eliminate the possibility that regulatory cells are involved. The investigator must specifically design experiments to look for these complex interactions in order to observe them. Further elucidation of the mechanisms by which Tcs and Ts cells mediate their opposing effects will likely come from comparisons of the protein structure and receptors for their soluble factors.
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Kelly, C.J., Neilson, E.G. Contrasuppression in autoimmunity. Immunol Res 7, 56–66 (1988). https://doi.org/10.1007/BF02918154
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DOI: https://doi.org/10.1007/BF02918154