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*
Istituto Dermopatico dell’Immacolata, IRCCS, Rome, Italy; and
Department of Dermatology, University of Aachen, Aachen, Germany
Allergic contact dermatitis (ACD) is the result of an exaggerated
immune reaction to haptens mediated by skin-homing T cells, but the
effector mechanisms responsible for the tissue damage are poorly
understood. Here we studied the capacity of distinct subsets of
hapten-specific T cells to induce apoptosis in autologous
keratinocytes. Skin- and blood-derived nickel-specific CD8+
T cytotoxic 1 (Tc1) and Tc2 clones as well as CD4+ Th1 and
Th2 expressed the cutaneous lymphocyte-associated Ag and exhibited
strong MHC-restricted cytotoxicity against nickel-coupled B
lymphoblasts, as detected by the [3H]TdR release assay.
Both Tc1 and Tc2 clones, but not CD4+ T cells, displayed a
significant cytotoxic activity against resting nickel-modified
keratinocytes. Following IFN-
treatment, keratinocytes expressed MHC
class II and ICAM-1 and became susceptible to Th1-mediated, but not
Th2-mediated, cytotoxicity. The molecules of the two major cytotoxic
pathways, Fas ligand (FasL) and perforin, were expressed by Tc1, Tc2,
and Th1 cells, whereas Th2 cells expressed only FasL. Experiments
performed in the presence of specific inhibitors of the perforin
(concanamycin A) and FasL (brefeldin A) pathway indicated that
perforin-mediated killing dominated in Tc1 and Tc2, and FasL-mediated
cytotoxicity prevailed in Th2 clones, with a more heterogeneous
behavior in the case of Th1 cells. Finally, perforin mRNA was expressed
in ACD lesional skin, as assessed by RT-PCR analysis. In aggregate, our
results indicate that keratinocytes can be target of multiple
hapten-specific CTL responses, that may have distinct roles in the
epidermal injury during ACD.
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