title: Induction of suppressors of cytokine signaling (SOCS) in the retina during experimental autoimmune uveitis (EAU): potential neuroprotective role of SOCS proteins.
abstract: Suppressors of cytokine signaling (SOCS) are implicated in immunopathogenic mechanisms of autoimmune diseases. We show here that SOCS expression in retina is temporarily correlated with progression of experimental autoimmune uveitis (EAU), an organ-specific autoimmune disease that serves as model of human uveitis. Peak of EAU correlates with highest SOCS genes expression while disease resolution coincides with their down-regulation. Surprisingly, SOCS5 is constitutively expressed in retina. SOCS5 expression increases significantly during EAU and remains elevated even after disease resolution. Our data suggest that cytokine-inducible SOCS members may be involved in negative regulation of inflammatory cytokines activities during EAU, while constitutively expressed SOCS5 may have neuroprotective functions.
authors.affiliation: Experimental Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Building 10, Room 10N116, 10 Center Drive, Bethesda, Maryland 20892-1857, USA.
authors.forename: H
authors.initials: H
authors.lastname: Takase
authors.forename: C-R
authors.initials: CR
authors.lastname: Yu
authors.forename: X
authors.initials: X
authors.lastname: Liu
authors.forename: C
authors.initials: C
authors.lastname: Fujimoto
authors.forename: I
authors.initials: I
authors.lastname: Gery
authors.forename: C E
authors.initials: CE
authors.lastname: Egwuagu
mesh_terms: D000818:Animals; D015153:Blotting, Western / Q000379:methods; D015704:CD4 Antigens / Q000378:metabolism; D049109:Cell Proliferation; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D024202:Electrophoretic Mobility Shift Assay / Q000379:methods; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D015870:Gene Expression / Q000187:drug effects; D051379:Mice; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000096:biosynthesis; D012160:Retina / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D012177:Retinol-Binding Proteins; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D015398:Signal Transduction / Q000502:physiology*; D050826:Suppressor of Cytokine Signaling Proteins / Q000494:pharmacology / Q000627:therapeutic use*; D013601:T-Lymphocytes / Q000378:metabolism; D013997:Time Factors; D014605:Uveitis / Q000139:chemically induced / Q000378:metabolism* / Q000517:prevention & control; D000099214:Retinol-Binding Proteins, Interstitial
chemical_list: D015704:CD4 Antigens; D016207:Cytokines; D018696:Neuroprotective Agents; D012333:RNA, Messenger; D012177:Retinol-Binding Proteins; D050826:Suppressor of Cytokine Signaling Proteins; C487847:Rbp3 protein, rat; D000099214:Retinol-Binding Proteins, Interstitial