Still more recently, the retinal antigen-induced uveitis models have allowed us to investigate the cellular and molecular

mechanisms that are involved in development and in

perpetuation of uveitis Based on these experimental animal studies, it appears that the initial events in the induction of uveitis may result from altered tolerance to retinal soluble
 
proteins, probably triggered by an infectious agent.  In most posterior uveitis, this alteration leads to T-lymphocyte mediated autoimmunity directed against retinal/ choroidal
proteins. An exciting finding in animal studies is that development of such autoimmunity can be prevented or suppressed by monoclonal antibodies to various T-cell surface
 [11]  
molecules  or major histocompatibility complex (MHC class II) antigens. There is also evidence to suggest that a limited number of T-cells with specific antigen receptors
 
recognise the intraocular antigens such as S-antigen or interphotoreceptor retinoid binding protein (IRBP) which are known to play some role in perpetuation of uveitis.
Elucidation of such antigen specific cellular and molecular changes promise a more specific manipulation of the immune system for treating autoimmune disorders.

Even though these new and exciting treatment possibilities may become available in the near future, for the appropriate management of uveitis today, it is important to recognise
and differentiate infectious cases from noninfectious autoimmune uveitis. Management of infectious uveitis is fairly straightforward; these cases are treated with appropriate
antimicrobial agents, with or without corticosteroids.The noninfectious and nontraumatic uveitis cases need to be identified prior to administration of anti-inflammatory or
immunosuppressive agents such as cyclophosphamide and cyclosporin A, and these are the ones that require a clear understanding of the autoimmune process that can lead
to uveitis.

Many factors must be taken into consideration when deciding when and how to treat noninfectious uveitis patients. A solid understanding of the natural history of a particular
uveitis entity is mandatory to avoid exposing the patient to unnecessary, excessive, or inappropriate treatment. A well- documented 'treatment response' history should be
considered when developing a fresh treatment strategy. Although symptoms can be useful parameters for judging treatment efficacy, in some instances, for example floaters,
they need not be pursued to extinction. The presence of inflammation alone is not always an indication for treatment. For example, a patient who has intermediate uveitis (pars
planitis) with moderate vitreous cells but with a visual acuity of 20/25 does not require treatment. Likewise, a patient who has Fuchs' heterochromic iridocyclitis should not be
given intensive topical corticosteroid treatment, as this will merely hasten the development of cataract. On the other hand, a patient who has juvenile rheumatoid arthritis and
chronic flare alone does not need corticosteroid medications, but may require chronic mydriatic therapy to prevent the development of posterior synechiae. In all instances, a
risk-benefit analysis should be made, and therapy should be instituted only when the benefits of such therapy outweigh the potential complications.