Abstract
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.
Current Molecular Medicine
Title:Ocular Inflammatory Diseases: Molecular Pathogenesis and Immunotherapy
Volume: 15 Issue: 6
Author(s): C.E. Egwuagu, L. Sun, S.-H. Kim and I.M. Dambuza
Affiliation:
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.
Abstract: 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.
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Cite this article as:
Egwuagu C.E., Sun L., Kim S.-H. and Dambuza I.M., Ocular Inflammatory Diseases: Molecular Pathogenesis and Immunotherapy, Current Molecular Medicine 2015; 15 (6) . https://dx.doi.org/10.2174/1566524015666150731095426
DOI https://dx.doi.org/10.2174/1566524015666150731095426 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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