For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
48
views
67
references
 Top references
cited by
34
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      157
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Sympathetic ophthalmia: to the twenty-first century and beyond

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Sympathetic ophthalmia is a rare bilateral granulomatous inflammation that follows accidental or surgical insult to the uvea of one eye. Onset of sympathetic ophthalmia can be insidious or acute, with recurrent periods of exacerbation. Clinical presentation shows mutton-fat keratic precipitates, choroidal infiltrations, and Dalen-Fuchs nodules. Histopathology reveals diffuse or nodular granulomatous inflammation of the uvea. Prevention and treatment strategies for sympathetic ophthalmia are currently limited to two modalities, enucleation of the injured eye and immunosuppressive therapy, aimed at controlling inflammation. The etiology and pathophysiology of the disease is still unclear but is largely thought to be autoimmune in nature. Recent insight on the molecular pathology of the disease as well as developments in imaging technology have furthered both the understanding on the autoimmune process in sympathetic ophthalmia and the targeting of prevention and treatment strategies for the future.

          Related collections

          Most cited references67

          • Record: found
          • Abstract: found
          • Article: not found

          Gelatinase B: a tuner and amplifier of immune functions.

          Ghislain Opdenakker, Philippe Van den Steen, Jo Van Damme (2001)
          Gelatinase B (matrix metalloproteinase-9) is a secreted multidomain enzyme that is important for the remodeling of the extracellular matrix and the migration of normal and tumor cells. It cleaves denatured collagens (gelatins) and type IV collagen, which is present in basement membranes. In the immune system, this cleavage helps lymphocytes and other leukocytes to enter and leave the blood and lymph circulations. Gelatinase B also cleaves myelin basic protein and type II gelatins, and this clipping leads to remnant epitopes that generate autoimmunity, the so-called REGA model of autoimmunity. Recently, gelatinase B has been found to process cytokines and chemokines, resulting in skewed immune functions. Therefore, gelatinase B, often considered as a pure effector molecule, acts as a switch and catalyst in both innate and specific immunity, and constitutes a prototypic example of the regulation of immune functions by proteolysis.
          Article 0 comments Cited 76 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Human alphaA- and alphaB-crystallins bind to Bax and Bcl-X(S) to sequester their translocation during staurosporine-induced apoptosis.

            Y. Mao, Anny H Xiang, J. Liu … (2004)
            AlphaA- and alphaB-crystallins are distinct antiapoptotic regulators. Regarding the antiapoptotic mechanisms, we have recently demonstrated that alphaB-crystallin interacts with the procaspase-3 and partially processed procaspase-3 to repress caspase-3 activation. Here, we demonstrate that human alphaA- and alphaB-crystallins prevent staurosporine-induced apoptosis through interactions with members of the Bcl-2 family. Using GST pulldown assays and coimmunoprecipitations, we demonstrated that alpha-crystallins bind to Bax and Bcl-X(S) both in vitro and in vivo. Human alphaA- and alphaB-crystallins display similar affinity to both proapoptotic regulators, and so are true with their antiapoptotic ability tested in human lens epithelial cells, human retina pigment epithelial cells (ARPE-19) and rat embryonic myocardium cells (H9c2) under treatment of staurosporine, etoposide or sorbitol. Two prominent mutants, R116C in alphaA-crystallin and R120G, in alphaB-crystallin display much weaker affinity to Bax and Bcl-X(S). Through the interaction, alpha-crystallins prevent the translocation of Bax and Bcl-X(S) from cytosol into mitochondria during staurosporine-induced apoptosis. As a result, alpha-crystallins preserve the integrity of mitochondria, restrict release of cytochrome c, repress activation of caspase-3 and block degradation of PARP. Thus, our results demonstrate a novel antiapoptotic mechanism for alpha-crystallins. 2004
            Article 0 comments Cited 65 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Monocyte chemoattractant protein-1 regulates adhesion molecule expression and cytokine production in human monocytes.

              G Frendl, Andrew Graves, D I Beller … (1992)
              Monocytes play a critical role in defending the host against foreign organisms and in regulating the behavior of other cells. Monocytes circulate as nonadherent cells in the blood and migrate as adherent cells through tissues. Adhesion molecules mediate not only cell adhesion, but also migration, phagocytosis, and many other adhesion-dependent functions. Monocyte chemoattractant protein-1 (MCP-1) is thought to be responsible for monocyte recruitment in acute inflammatory conditions and may be an important mediator in chronic inflammation. In this study, immunofluorescence flow cytometry was used to determine whether MCP-1 can regulate the cell surface expression of adhesion molecules, particularly beta-2 and alpha-4 integrins and the leukocyte adhesion molecule-1. We found that MCP-1 induced expression of CD11c (p150,95 alpha-subunit) and CD11b (Mac-1 alpha-subunit), and caused little or no change of CD11a (lymphocyte function-associated Ag-1 alpha-subunit), very late activation Ag-4, or leukocyte adhesion molecule-1. We demonstrated that antibodies to beta-2 and alpha-4 integrins inhibited MCP-1-induced monocyte chemotaxis. We also showed that MCP-1 is capable of inducing IL-1 and IL-6, but not TNF production of monocytes. These results indicate that MCP-1 is not only a chemoattractant but also a novel cytokine with the capacity to regulate several parameters of monocyte function.
              Article 0 comments Cited 43 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Xi K Chu
                Chi-Chao Chan
                Journal
                Journal ID (nlm-ta): J Ophthalmic Inflamm Infect
                Journal ID (iso-abbrev): J Ophthalmic Inflamm Infect
                Title: Journal of Ophthalmic Inflammation and Infection
                Publisher: Springer
                ISSN (Electronic): 1869-5760
                Publication date Collection: 2013
                Publication date (Electronic): 1 June 2013
                Volume: 3
                Page: 49
                Affiliations
                [1 ]Immunopathology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, 10 Center Drive, Room 10N103, Bethesda, MD 20892, USA
                Article
                Publisher ID: 1869-5760-3-49
                DOI: 10.1186/1869-5760-3-49
                PMC ID: 3679835
                PubMed ID: 23724856
                SO-VID: 67c958ab-14a0-4c55-907e-e3b39bedc315
                Copyright © Copyright ©2013 Chu and Chan; licensee Springer.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 2 April 2013
                Date accepted : 23 May 2013
                Categories
                Subject: Review

                ScienceOpen disciplines: Ophthalmology & Optometry
                Keywords: sympathetic ophthalmia,dalen-fuchs nodules,inflammation,enucleation,corticosteroids,ocular imaging
                Data availability:
                ScienceOpen disciplines: Ophthalmology & Optometry
                Keywords: sympathetic ophthalmia, dalen-fuchs nodules, inflammation, enucleation, corticosteroids, ocular imaging

                Comments

                Comment on this article

                scite_

                Similar content157

                See all similar

                Cited by34

                See all cited by

                Most referenced authors390

                See all reference authors