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C. E. Thirkill; Autoimmune Retinal Vasculitis. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1539.
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Aberrant immunologic activity in retinal vasculitis has been of interest for many years stemming from the earliest observations of abnormal antibody reactions with the retinal vasculature, and its response to immuno-modulation, but the lack of any recognized autoantigen makes it difficult to prove autoimmunity. Preliminary studies on the immunologic activity of idiopathic retinopathy patients by Indirect Fluorescent Antibody assay (IFA) on sectioned rhesus monkey eye lead to the selection of twelve with antibody activity involving components of the retinal choroidal vascular bed. Western blots on retina and in vitro cultured Human Umbilical Vein Endothelial Cells (HUVEC) and Human Aortic Endothelial Cells (HAEC) identified an immunologic commonality involving a 55 kd protein This reaction was interpreted to indicate that each patient had experienced a common source of sensitization. 55 kd reactive sera were subjected to further analysis on the antigens of Escherichia. coli prompted by previous findings made in this and other laboratories that implicate certain strains of E. coli in the induction of some rare forms of retinal hypersensitivity.
Preliminary findings made by IFA on sectioned rhesus monkey eye, and Western blots of retina, HUVEC and HAEC were pursued further using Western blots of an E.coli previously isolated from one of the 55 kd reactive patients who has a history of urinary tract infection.
Western blots of the E.coli probed with sera from 55 kd reactive patients revealed an antigen-antibody reaction with a protein component of equivalent size; 55 kd. Antibodies eluted from the 55 kd reactive site of the E. coli blot were found to relocate to the 55 kd region of Western blots of retina, HUVEC, HAEC, and the vascular bed of sectioned rhesus monkey eye.
Infection with an E coli expressing a 55 kd protein antigen sharing an immunologic relationship with a vascular antigen could conceivably incite an autoimmune vasculitis. It is understood that because the cultured vascular endothelia used in this study are not from the eye the 55 kd reaction cannot be said to be specific for retinal vasculitis, even though the patients involved are producing antibodies that bind ocular vasculature. It’s possible that antibody activity with the 55 kd vascular antigen is induced in response to vascular inflammation distant from the eye. If this proves to be the case the 55 kd antigen will be exposed as an immunologic commonality of increased interest one capable of providing the means for the rapid, non-invasive diagnosis of occult vascular inflammations through the introduction of a test involving a recognized vascular component.
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