Contact sensitivity (CS) is a form of delayed‐type hypersensitivity to haptens applied epicutaneously and is thought to be mediated, like classical delayed‐type hypersensitivity responses, by CD4+ T helper‐1 cells. The aim of this study was to identify the effector T cells involved in CS. We studied CS to the strongly sensitizing hapten dinitrofluorobenzene (DNFB) in mice rendered deficient by homologous recombination in either major histocompatibility complex (MHC) class I, MHC class II, or both, and which exhibited deficiencies in, respectively, CD8+, CD4+, or both, T cells. MHC class I single‐deficient and MHC class I/class II double‐deficient mice, both of which have a drastic reduction in the number of CD8+ T cells, were unable to mount a CS response to DNFB. In contrast, both MHC class II‐deficient mice and normal mice treated with an anti‐CD4 monoclonal antibody (mAb) developed exaggerated and persistent responses relative to heterozygous control littermates. Furthermore, anti‐CD8 mAb depletion of class II‐deficient mice totally abolished their ability to mount an inflammatory response to DNFB. Removal of residual CD4+ T cells in class II‐deficient mice by anti‐CD4 mAb treatment did not diminish the intensity of CS. These data clearly demonstrate that class I‐restricted CD8+ T cells are sufficient for the induction of CS to DNFB, and further support the idea that MHC class II‐restricted CD4+ T cells down‐regulate this inflammatory response.

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The effects of thalidomide on chemotaxis of normal human peripheral blood PMN leukocytes have been studied in vitro. The chemotaxis factor was generated by interacting normal human serum with bovine gamma globulin-antibovine-gamma globulin immune complexes. At concentrations of 1, 10, and 100 microgram/ml, thalidomide failed to inhibit the chemotactic factor. At the same concentrations, erythromycin caused a marked inhibition of chemotaxis. Pre-incubation of PMNs with thalidomide or erythromycin caused a marked, dose-independent inhibition of chemotaxis. Random mobility did not appear to be affected. Inhibition of PMN chemotactic ability by thalidomide may account for its ability to improve inflammatory dermatoses, such as aphthosis.