The presence of macrophage migration inhibitory factor in human trabecular meshwork and its upregulatory effects on the T helper 1 cytokine.

PURPOSE: To investigate the expression and secretion of macrophage migration inhibitory factor (MIF) in human trabecular meshwork (HTM) and evaluate its role in ocular inflammation. METHODS: Tissue samples of HTM cells were isolated from donor human eyes or corneoscleral buttons, and the HTM cells were cultured. The expression of MIF on HTM cells was evaluated by RT-PCR, Western blot analysis, and ELISA. T-cell clones (TCCs) were established from ocular infiltrating cells of patients with uveitis. ELISA was used to evaluate the pathologic role of MIF, in relation to regulatory effects on cytokine production by T cells. RESULTS: MIF was detected in the HTM by RT-PCR and Western blot analysis. MIF was also shown by ELISA to be secreted by the HTM cells in culture. The HTM supernatant enhanced IFN-gamma production by TCCs, but not IL-10; and these effects were neutralized by anti-MIF antibodies. Similarly, recombinant MIF enhanced the IFN-gamma production by the TCCs. CONCLUSIONS: MIF is expressed and secreted in the HTM, and MIF has the capacity to enhance T helper 1 cytokines and may play a role as an inflammatory cytokine in the eye.