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A Soluble Factor Produced by Lamina Propria Mononuclear Cells Is Required for TNF- Enhancement of IFN- Production by T Cells¹

Cedars-Sinai Inflammatory Bowel Disease Center, Los Angeles, CA 90048

The role of TNF- in the mucosal inflammation of Crohn’s disease has been demonstrated by the prolonged clinical responses and/or remissions among patients receiving i.v. infusion of anti-TNF-. A correlation between TNF- and elevated IFN- production is suggested by the reduction in the number of IFN- producing lamina propria mononuclear cells (LPMC) found in colonic biopsies from anti-TNF--treated patients. The aim of this study was to define the mechanism of TNF--augmented mucosal T cell IFN- production. In this paper we present evidence that cultured LPMC secrete a factor which acts on preactivated T cells in concert with TNF- to augment IFN- production. This activity is independent of IL-12 and IL-18, the well-documented potentiators of IFN- expression, and is not produced by PBMC. Peripheral blood PHA-activated T cells incubated in supernatants from LPMC became responsive to TNF- by increasing IFN- output upon stimulation. These results are consistent with a model in which LPMC, but not PBMC, release an unidentified substance when cultured in vitro with low dose IL-2. This substance can act on preactivated peripheral T cells, as well as on lamina propria T cells, conditioning them to respond to TNF- by increased IFN- secretion upon stimulation. Expression of this factor in the gut mucosa could contribute to up-regulation of the Th1 response in the presence of TNF-, and could be important for mucosal immunoregulation.

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