Uveitis is a diverse group of potentially sight-threatening intraocular inflammatory
diseases of infectious or autoimmune etiology and accounts for more than 10% of severe
visual handicaps in the United States. Pathology derives from the presence of inflammatory
cells in the optical axis and sustained production of cytotoxic cytokines and other immuneregulatory
proteins in the eye. The main therapeutic goals are to down-regulate the immune
response, preserve the integrity of the ocular architecture and eventually eliminate the
inciting uveitogenic stimuli. Current therapy is based on topical or systemic corticosteroid with
or without second line agents and serious adverse effects of these drugs are the impetus for development of
less toxic and more specific therapies for uveitis. This review summarizes the pathophysiology of uveitis,
molecular mechanisms that regulate the initiation and progression of uveitis and concludes with emerging
strategies for the treatment of this group of potentially blinding diseases.
Keywords: B cell therapy, IL-12 cytokines, IL-35-expressing Breg cell (i35-Breg), interleukin 35 (IL-35), regulatory
B cells (Breg), therapeutic cytokines, uveitis.
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