The pathogenic mechanisms underlying
uveitis syndromes continue to be evaluated using animal models and in the clinical setting. As the complex interactions between ocular immune cells, proinflammatory
cytokines,
chemokines and cellular adhesion molecules are uncovered, targeted
therapies directed against these immune mediators will continue to be developed. Traditional immunosuppressive medications, such as
corticosteroids and
steroid-sparing
immunomodulatory agents, have demonstrated efficacy in the treatment of uveitic syndromes, but side effects and
drug toxicities often limit the use of these medications. The
biologic agents, a newer class of medications, target specific immune pathways and have demonstrated efficacy in rheumatologic, dermatologic and neurologic conditions.
Biologic therapies (e.g.,
TNF-alpha inhibitors and
IL-2 receptor inhibitor) targeting ocular immune
cell surface receptors,
cytokines and
chemokines continue to be developed and have shown promise in the treatment of
uveitis and ocular inflammatory diseases. Clinical and basic aspects of
monoclonal antibody therapy for
uveitis are presented in this review. Additional studies are needed to further evaluate the role of
monoclonal antibodies in the therapeutic armamentarium for
uveitis.