Using conventional histological (light and electron microscopic examinations), immunohistological (immunofluorescent and immunoperoxidase), and molecular histological (in situ hybridisation and polymerase chain reaction (PCR) in situ hybridisation) techniques, the immunopathology of uveitis has been studied using inflamed ocular tissue. 1–4 The findings usually provide helpful information in the diagnosis and therapy of uveitis. The immunopathology of uveitis allows the visualisation of the morphological interaction in the eye at the time the specimen is obtained. This information also helps in the understanding of the immunopathogenesis of ocular inflammation. Three main aspects of pathological examinations are analysed. Firstly, the morphology of the ocular specimen illustrates the lesions and specific localisations within the eye. These include inflammatory exudate in the anterior chamber, known as hypopyon, commonly located at the inferior angle, inflammatory cellular infiltration in the cornea (keratitis), the uvea (focal or diVuse iritis, cyclitis, iridocyclitis, choroiditis), the retina (retinitis), the vitreous (vitritis or abscess), the sclera (scleritis), and inflammation surrounding the lens or its remnants. The following terms indicate certain pathological findings in the eye. Endophthalmitis occurs when ocular inflammation is confined to three or more tissues inside the eye. Panophthalmitis, on the other hand, indicates that ocular inflammation involves all layers of the eye including the sclera. Anterior uveitis is ocular inflammation in the cornea, the iris, and the ciliary body. Posterior uveitis is ocular inflammation in the choroid, the retina, and the vitreous. Panuveitis is ocular inflammation in both anterior and posterior segments of the eye.

Secondly, agents that induce inflammation. Biological, chemical, or physical stimuli can induce ocular inflammation. Various infectious micro-organisms including bacteria, viruses, fungi, and parasites are capable of triggering diVerent degrees of inflammatory response. Several ocular proteins, such as retinal soluble antigen (S-Ag), 5 interphotoreceptor retinoid binding protein (IRBP), 6 and uveal melanin associated proteins, 7 are autoantigens inside the eye. These potent antigens are known not only to induce ocular inflammation in various animal models, 5–7 but also may be involved in human uveitides based on clinical studies. 8–10 Cellular responses to S-Ag, IRBP, and their peptides have been reported in patients with uveitis. 11–13 Antiretinal autoantibodies have been shown in the sera of uveitic patients. 14 15 Some investigators have considered that sympathetic ophthalmia and Vogt–Koyanagi–Harada (VKH) syndrome reflect autoimmunity against choroidal melanocytes. 16–18 Recently, two peptides derived from the human S-Ag have been found to bind eYciently to HLAA29, the predisposing allele for birdshot retinopathy. 19 This finding demonstrates the implication of T cell epitopes from retinal autoantigens in birdshot retinopathy. Trauma and foreign bodies can elicit an inflammatory reaction