THE CELLULAR IMMUNE DEFECT IN CHRONIC MUCOCUTANEOUS CANDIDIASIS

Cutaneous hypersensitivity of the delayed type can be divided into three sequential phases or steps: (1) antigen recognition and/or processing; (2) production of chemotactic factors or mediators which attract unsensitised cells (monocytes) to the site of the reaction, and (3) changes in the vascular endothelium and "activation" of the monocytes resulting in perivascular mononuclear cell infiltration at the site of antigen injection, interpreted clinically as erythema and induration. Three patients with chronic mucocutaneous candidiasis had generalised cutaneous anergy. Paradoxically, their lymphocytes respond in vitro to phytohæmagglutinin, Candida antigen, and allogeneic cells, indicating an intact antigen recognition and processing phase. Two of the three patients were given lymphocytes from healthy donors, and this resulted in temporary reversal of the generalised cutaneous anergy. Since in such passive-transfer experiments only a small percentage of donor cells are found in the resultant delayed hypersensitivity reaction, the restoration of reactivity implies an adequate population of host cells capable of expressing the inflammatory and clinical events of the cutaneous reaction. The cutaneous anergy in these three patients then seems to result from a deficiency of mediator production, probably migration inhibitory factor, or the presence of an inhibitor to this factor or to other mediators.