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A Selective Role for the TNF p55 Receptor in Autocrine Signaling following IFN- Stimulation in Experimental Autoimmune Uveoretinitis¹

Claudia J. Calder^*, Lindsay B. Nicholson^2,*, and Andrew D. Dick

^* Department of Pathology and Microbiology, University of Bristol, Bristol, United Kingdom; and Clinical Sciences at South Bristol, Bristol Eye Hospital, Bristol, United Kingdom

IFN- stimulates macrophage activation and NO production, which leads to destruction of the retina in experimental autoimmune uveoretinitis. In this study, we investigate the mechanism of disease resistance in TNF p55 receptor-deficient animals. We show that although T cell priming is relatively unaffected, macrophages lacking the TNF p55 receptor fail to produce NO following IFN- stimulation because of a requirement for autocrine TNF- signaling through the TNF p55 receptor. In contrast to the impaired activation of NO synthesis, MHC class II up-regulation was indistinguishable in wild-type and TNFRp55^–/– mice stimulated with IFN-. These defects could be overcome by stimulating macrophages with LPS. Together, these results show that selected aspects of IFN- activation are controlled by autocrine secretion of TNF-, but that this control is lost in the presence of signals generated by pathogen-associated molecular patterns recognizing receptors.

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