title: Constitutive neuronal expression of the immune regulator, programmed death 1 (PD-1), identified during experimental autoimmune uveitis.
abstract: OBJECTIVE
  Programmed death-1 (PD-1) ligation downregulates active lymphocyte responses. The authors tested whether PD-1 or its ligands are expressed in the posterior segment during active intraocular inflammation.
  
  
  METHODS
  Experimental autoimmune uveitis (EAU) was induced using interphotoreceptor retinoid-binding protein (IRBP 161-180). Ocular inflammation was evaluated by histology and expression of PD-1 ligand tested by immunohistochemistry. PD-1 expression was evaluated by immunohistochemistry, RT-PCR, and Western immunoblotting.
  
  
  RESULTS
  Using immunohistochemistry, PD-1, but not its ligands, was constitutively expressed in retinal neurons of naive mouse retina. Both PD-1 and its ligands were observed, as expected, in sites of active inflammation.
  
  
  CONCLUSIONS
  PD-1 and its ligands were expressed in sites of active inflammation, in accordance with many other models of inflammatory disease. Surprisingly, PD-1, not previously described outside the immune system, was constitutively expressed in retinal neurons, raising the possibility that PD-1 signaling may be important for neuronal function in the absence of an inflammatory insult.
authors.affiliation: Department of Ophthalmology, Jules Stein Institute, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA.
authors.forename: Ling
authors.initials: L
authors.lastname: Chen
authors.forename: Vicky
authors.initials: V
authors.lastname: Pai
authors.forename: Ralph
authors.initials: R
authors.lastname: Levinson
authors.forename: Arlene H
authors.initials: AH
authors.lastname: Sharpe
authors.forename: Gordon J
authors.initials: GJ
authors.lastname: Freeman
authors.forename: Jonathan
authors.initials: J
authors.lastname: Braun
authors.forename: Lynn K
authors.initials: LK
authors.lastname: Gordon
mesh_terms: D000818:Animals; D000954:Antigens, Surface / Q000235:genetics / Q000378:metabolism*; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism*; D001327:Autoimmune Diseases / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D018122:B7-1 Antigen / Q000235:genetics / Q000378:metabolism; D060890:B7-H1 Antigen; D015153:Blotting, Western; D001921:Brain / Q000378:metabolism; D004195:Disease Models, Animal; D005136:Eye Proteins; D007124:Immunoenzyme Techniques; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D010446:Peptide Fragments; D010455:Peptides / Q000235:genetics / Q000378:metabolism; D061027:Programmed Cell Death 1 Ligand 2 Protein; D061026:Programmed Cell Death 1 Receptor; D012333:RNA, Messenger / Q000378:metabolism; D012177:Retinol-Binding Proteins; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017422:Sequence Analysis, DNA; D015866:Uveitis, Posterior / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D000099214:Retinol-Binding Proteins, Interstitial
chemical_list: D000954:Antigens, Surface; D051017:Apoptosis Regulatory Proteins; D018122:B7-1 Antigen; D060890:B7-H1 Antigen; D005136:Eye Proteins; D008562:Membrane Glycoproteins; D010446:Peptide Fragments; D010455:Peptides; D061027:Programmed Cell Death 1 Ligand 2 Protein; D061026:Programmed Cell Death 1 Receptor; D012333:RNA, Messenger; D012177:Retinol-Binding Proteins; D000099214:Retinol-Binding Proteins, Interstitial; C498919:Cd274 protein, mouse; C491383:Pdcd1 protein, mouse; C556978:Pdcd1lg2 protein, mouse