title: Distribution of OX2 antigen and OX2 receptor within retina.
abstract: OBJECTIVE
  OX2 is a member of the immunoglobulin superfamily expressed on a broad range of tissues including neurons of the central and peripheral nervous systems, thymocytes, and endothelium. The recently identified OX2 receptor (OX2R) is restricted to the surfaces of myeloid lineage cells, including microglia. Functional data have implicated the OX2-OX2R interaction as a myeloid downregulatory signal. The purpose of this study was to determine the distribution and extent of expression of OX2 and its receptor within the retina, a tissue developed to restrain immune-mediated inflammatory damage.
  
  
  METHODS
  OX2 and OX2R monoclonal antibodies (mAbs) were used to determine OX2 and OX2R protein expression, respectively, by flow cytometry of isolated myeloid-derived cells from normal and inflamed rat retina and by immunohistochemistry of serial sections of rat retina. For comparison, distribution of OX2 was documented using species-specific monoclonal antibodies in mouse and human retina. No OX2R mAbs are available for mouse or human detection.
  
  
  RESULTS
  OX2 was expressed on retinal vascular endothelium and glial fibrillary acidic protein (GFAP)-negative neurons in retina and optic nerve and on a subpopulation of CD45(+) perivascular and juxtavascular cells. Within normal retina, OX2R was not detected on myeloid-derived cells. During experimental autoimmune uveoretinitis (EAU), expression of both OX2 and OX2R was noted on infiltrating leukocytes.
  
  
  CONCLUSIONS
  Taking these results of the distribution of OX2 in normal and OX2R in inflamed retina with other functional data of OX2-OX2R interaction, it is suggested that the OX2-OX2R interaction has the potential to contribute to a novel pathway that suppresses and limits immunologic inflammatory damage within the retina.
authors.affiliation: Division of Ophthalmology, University of Bristol, United Kingdom. a.dick@bristol.ac.uk
authors.forename: A D
authors.initials: AD
authors.lastname: Dick
authors.forename: C
authors.initials: C
authors.lastname: Broderick
authors.forename: J V
authors.initials: JV
authors.lastname: Forrester
authors.forename: G J
authors.initials: GJ
authors.lastname: Wright
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D000954:Antigens, Surface / Q000378:metabolism*; D001327:Autoimmune Diseases / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D004730:Endothelium, Vascular / Q000378:metabolism; D005136:Eye Proteins / Q000378:metabolism*; D005434:Flow Cytometry; D019084:Fluorescent Antibody Technique, Indirect; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D007124:Immunoenzyme Techniques; D008562:Membrane Glycoproteins / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000378:metabolism; D009900:Optic Nerve / Q000378:metabolism; D064446:Orexin Receptors; D051381:Rats; D011917:Rats, Inbred Lew; D043562:Receptors, G-Protein-Coupled; D018013:Receptors, Neuropeptide / Q000378:metabolism*; D012160:Retina / Q000378:metabolism* / Q000473:pathology; D012173:Retinitis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D012177:Retinol-Binding Proteins; D014605:Uveitis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D000099214:Retinol-Binding Proteins, Interstitial
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D000954:Antigens, Surface; D005136:Eye Proteins; D005904:Glial Fibrillary Acidic Protein; D008562:Membrane Glycoproteins; D064446:Orexin Receptors; D043562:Receptors, G-Protein-Coupled; D018013:Receptors, Neuropeptide; D012177:Retinol-Binding Proteins; D000099214:Retinol-Binding Proteins, Interstitial; C578626:HCRTR2 protein, human; C042739:antigens, CD200