Abstract
Epidermal spongiosis, invasion of mononuclear cells into the epidermis, and epidermal cell destruction are regular findings in allergic contact dermatitis. The mechanism(s) by which these changes occur is not known. We have examined the possibility that some of the pathological changes observed in allergic contact dermatitis could be accounted for by invasion of the epidermis by cytotoxic effector cells which recognize hapten-modified self-antigens and therein cause epidermal cell destruction. C3H and BALB/c mice were sensitized by epicutaneously applied 7% trinitrochlorobenzene (TNCB). 14days later spleen cells from these mice were stimulated in vitro to trinitrophenylated-(TNP-conjugated) syngeneic spleen cells and their responses were compared to the in vitro responses of spleen cells from unsensitized mice. After 5days of culture, effector cell activity was assayed on 51Cr-labeled TNP-conjugated syngeneic epidermal cells and on unconjugated epidermal cells. Cytotoxic activity was detected in the spleens of both mouse strains, but was greater in the C3H than the BALB/c strain. The cytotoxic effector cell activity was hapten specific in that spleen cells from TNCB sensitized mice did not cause lysis of fluorescein isothiocyanate (FITC) conjugated epidermal cells and spleen cells from FITC sensitized mice did not cause lysis of TNP-conjugated epidermal cells. No significant cytotoxic activity was detected on unconjugated epidermal cells. These findings suggest that destruction of the epidermis in allergic contact dermatitis may be contributed to by sensitized cytotoxic effector cells.
