Epidermal lesions of the GVHR: evaluation of the role of different MHC and non MHC loci and of the Ly-2+ and L3T4+ T lymphocytes.

Irradiated mice (750 rad) were injected with T-depleted bone marrow cells (BMC) and T lymphocytes in various combinations of T/host incompatibility. The epidermis was examined histologically and the incidence of two basic epidermal lesions of graft-vs-host disease (GVHD), the epidermal cell necrosis (ECN) and the lichenoid hyperplastic reaction (LR), were evaluated by a semi-quantitative evaluation. During the acute phase of GVH reaction (GVHR) (days 15 to 25), there was an obvious increase in ECN in reactions elicited by minor loci, whole major histocompatability complex (MHC) differences, or a MHC class I or II difference only. Allogeneic effect without T lymphocyte/epidermis incompatibility did not induce a significant incidence of ECN. Neither depletion of the Ly-2+ nor that of the L3T4+ T lymphocyte subset by treatment with monoclonal antibody (performed in vitro, before injection or also by treatment of the recipient) did prevent the occurrence of ECN, indicating that both T lymphocyte subsets are capable of initiating the epidermal cell damage. The LR was due mainly to the T lymphocytes of the L3T4+, Ly-2- helper phenotype. During chronic GVHR (after 35 days) elicited by either Ly-2+ or L3T4+ lymphocytes, ECN and LR were no longer evident, but the number of epidermal cells and especially the number of replicating cells among the epidermal cells were markedly reduced.