IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sohn, J.-H.
Right arrow Articles by Bora, N. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sohn, J.-H.
Right arrow Articles by Bora, N. S.
(Investigative Ophthalmology and Visual Science. 2000;41:4195-4202.)
© 2000 by The Association for Research in Vision and Ophthalmology, Inc.

Complement Regulatory Activity of Normal Human Intraocular Fluid Is Mediated by MCP, DAF, and CD59

Jeong-Hyeon Sohn1,3, Henry J. Kaplan1,3, Hye-Jung Suk1,3, Puran S. Bora2,3 and Nalini S. Bora1,3

1 From the Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, 2 Department of Medicine, Division of Cardiology, St. Louis University Medical Center, St. Louis, Missouri.

PURPOSE. To identify the molecules in normal human intraocular fluid (aqueous humor and vitreous) that inhibit the functional activity of the complement system.

METHODS. Aqueous humor and vitreous were obtained from patients with noninflammatory ocular disease at the time of surgery. Samples were incubated with normal human serum (NHS), and the mixture assayed for inhibition of the classical and alternative complement pathways using standard CH50 and AH50 hemolytic assays, respectively. Both aqueous humor and vitreous were fractionated by microconcentrators and size exclusion column chromatography. The inhibitory molecules were identified by immunoblotting as well as by studying the effect of depletion of membrane cofactor protein (MCP), decay-accelerating factor (DAF), and CD59 on inhibitory activity.

RESULTS. Both aqueous humor and vitreous inhibited the activity of the classical pathway (CH50). Microcentrifugation revealed the major inhibitory activity resided in the fraction with an Mr >= 3 kDa. Chromatography on an S-100-HR column demonstrated that the most potent inhibition was associated with the high-molecular-weight fractions (>=19.5 kDa). In contrast to unfractionated aqueous and vitreous, fractions with an Mr >= 3 kDa also had an inhibitory effect on the alternative pathway activity (AH50). The complement regulatory activity in normal human intraocular fluid was partially blocked by monoclonal antibodies against MCP, DAF, and CD59. Immunoblot analysis confirmed the presence of these three molecules in normal intraocular fluid.

CONCLUSIONS. Our results demonstrate that normal human intraocular fluid (aqueous humor and vitreous) contains complement inhibitory factors. Furthermore, the high-molecular-weight factors appear to be the soluble forms of MCP, DAF, and CD59.




This article has been cited by other articles:


Home page
IOVSHome page
P. Jha, B. Matta, V. Lyzogubov, R. Tytarenko, P. S. Bora, and N. S. Bora
Crucial Role of Apoptosis in the Resolution of Experimental Autoimmune Anterior Uveitis
Invest. Ophthalmol. Vis. Sci., November 1, 2007; 48(11): 5091 - 5100.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
N. S. Bora, S. Kaliappan, P. Jha, Q. Xu, B. Sivasankar, C. L. Harris, B. P. Morgan, and P. S. Bora
CD59, a Complement Regulatory Protein, Controls Choroidal Neovascularization in a Mouse Model of Wet-Type Age-Related Macular Degeneration
J. Immunol., February 1, 2007; 178(3): 1783 - 1790.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
J. Hori, M. Wang, M. Miyashita, K. Tanemoto, H. Takahashi, T. Takemori, K. Okumura, H. Yagita, and M. Azuma
B7-H1-Induced Apoptosis as a Mechanism of Immune Privilege of Corneal Allografts
J. Immunol., November 1, 2006; 177(9): 5928 - 5935.
[Abstract] [Full Text] [PDF]


Home page
IOVSHome page
M. Engelbert and M. S. Gilmore
Fas Ligand but Not Complement Is Critical for Control of Experimental Staphylococcus aureus Endophthalmitis
Invest. Ophthalmol. Vis. Sci., July 1, 2005; 46(7): 2479 - 2486.
[Abstract] [Full Text] [PDF]


Home page
IOVSHome page
M. S. Gregory, S. Koh, E. Huang, R. R. Saff, A. Marshak-Rothstein, S. Mukai, and B. R. Ksander
A Novel Treatment for Ocular Tumors Using Membrane FasL Vesicles to Activate Innate Immunity and Terminate Immune Privilege
Invest. Ophthalmol. Vis. Sci., July 1, 2005; 46(7): 2495 - 2502.
[Abstract] [Full Text] [PDF]


Home page
IOVSHome page
J. Y. Niederkorn, E. Mayhew, J. Mellon, and S. Hegde
Role of Tumor Necrosis Factor Receptor Expression in Anterior Chamber-Associated Immune Deviation (ACAID) and Corneal Allograft Survival
Invest. Ophthalmol. Vis. Sci., August 1, 2004; 45(8): 2674 - 2681.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
P. S. Bora, Z. Hu, T. H. Tezel, J.-H. Sohn, S. G. Kang, J. M. C. Cruz, N. S. Bora, A. Garen, and H. J. Kaplan
Immunotherapy for choroidal neovascularization in a laser-induced mouse model simulating exudative (wet) macular degeneration
PNAS, March 4, 2003; 100(5): 2679 - 2684.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2000 by the Association for Research in Vision and Ophthalmology