In order to investigate the biologic significance of HLA-DR expression by human keratinocytes, we have examined the possibility that DR-positive keratinocytes become alloantigen presenting cells for resting T cells in the presence of interleukin-2. Using this system, gamma interferon-treated, DR-positive keratinocytes stimulate the proliferation of allogeneic, resting T cells approximately 3-fold whereas non-gamma interferon-treated, DR-negative keratinocytes do not. Because a monoclonal antibody against recombinant gamma interferon inhibits this proliferation, the stimulation is dependent on pre-incubation with gamma interferon. By contrast, since the stimulation is not inhibited by a monoclonal antibody against HLA-DR, it is not clear that the stimulation is due to class II antigen expression by keratinocytes. To rule out that gamma interferon increases the expression of class I antigens, leading to stimulation of resting T cells on that basis, we determined whether gamma interferon treatment enhances class I antigen expression by keratinocytes. The lymphokine treated cells did not demonstrate more class I antigen expression than untreated keratinocytes. Thus, the observed stimulation of allogeneic, resting T cells by gamma interferon-treated keratinocytes in the presence of IL-2 is not due to increased class I antigen expression but is due to other cell surface antigen(s) induced by recombinant gamma interferon treatment. These results suggest that gamma interferon-exposed keratinocytes in the presence of interleukin-2 may augment the activation of resting T lymphocytes and, in this manner, may contribute to cutaneous inflammation.
Antibodies, Monoclonal Cells, Cultured