T Cell Abnormalities in Atopic Dermatitis Patients: Imbalances in T Cell Subpopulations and Impaired Generation of Con A-induced Suppressor Cells

It has been hypothesized, but not yet proven, that T cell dysfunction is operative in the pathogenesis of atopic dermatitis. In order to test this hypothesis, we assessed different quantitative and functional parameters indicative of T cell reactivity in atopic dermatitis patients and, for control purposes, in age-matched normal individuals. We found that mononuclear cells from atopic dermatitis patients proliferated in response to various concentrations of the mitogens concanavalin A (Con A) and phytohemagglutinin as well as did mononuclear cells from controls. However, atopic dermatitis patients, regardless of their clinical characteristics, have a significant decrease in the relative percentages of circulating total E rosette forming cells. The reduction in total T cell percentages may be due, in part, to a highly significant reduction in the percentages of Fc-IgG receptor bearing T cells (Tγ cells) that we found in atopic dermatitis patients at every level of clinical involvement. Fc-IgM receptor bearing T cell values (Tμ cells) were found to be within the normal range. A defect related to the severity of the eczematous eruption was revealed when we investigated the capability of Con A-activated mononuclear cells from either atopics or normals to suppress mitogenic responses of autologous and allogeneic mononuclear cells. We found that cells from atopic dermatitis patients with wide-spread clinical involvement could not be educated to express suppressor signals as effectively as could cells from clinically inactive patients or normal healthy individuals. Based on these findings, we propose that a regulatory cell defect operating at the T cell level participates in the pathogenesis of various aspects of atopic dermatitis.