ABSTRACT
Retinal destruction during inflammatory responses are mediated by non-specific
infiltration of mononuclear cells and polymorphonuclear cells. In particular
macrophages which are predominant in the retinal cell infiltrate during disease
course of experimental models of automimmune retinal inflammation are
adaptable in their behaviour. Cytokine conditioning of macrophage behaviour is
well recognised, for example when maximal retinal destruction occurs during
experimental autoimmune uveoretinitis, macrophages generate nitrite. Nitrite
production is dependent upon operational Tumour Necrosis Factor-alpha (TNFa) p55 receptor signalling following interferon-gamma activation of macrophage.
INTRODUCTION
