Immunity humoral, retinoid effects

Further direct proof that retinoid-effected inhibition of tumor growth and lower incidence of tumors is due to stimulation of the immune system rather than by toxic effects of retinoid directly on the tumor was provided by the experiments of Patek et al. (1979). Animals were thymectomized, lethally irradiated, and reconstituted with fetal liver (ATxFL) in order to compromise their humoral and cell-mediated immune system by the elimination of T cells. Under these conditions it was demonstrated that ATxFL mice are not able to suppress the growth of S91 or L33 tumor growth when treated with retinoid. Therefore, for these two tumor models, it seems highly likely that the retinoid effect requires the participation of immunocompetent cells, in particular, T cells. 

Because it appears that retinoids may act in an immunostimulatoiy capacity, at least in some tumor systems, the next question that can be asked is whether humoral, i.e., antibody-mediated, or cellular immunity is stimulated. In particular, one can ask specifically which immunological cell types are influenced by retinoids. Experiments with this objective require in vivo and in vitro immune response assays, cell culture techniques, and cell separation procedures that are quite laborious. Consequently, there are only a small number of reports that adequately deal with this question, albeit, only in a rather preliminary way. In the following sections, we attempt to evaluate the effects of retinoids on the two major arms of the immune system— the humoral and the cell-mediated. This division may seem somewhat artificial because of the overlap between the two systems, but it does provide some classification, enabling us to evaluate more easily the work in this field. 

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