title: Interaction of copolymer-1-activated T cells and microglia in retinal ganglion cell protection.
abstract: BACKGROUND
  The interaction of copolymer-1-activated T cells and microglia on retinal ganglion cells survival in vitro was explored.
  
  
  METHODS
  Copolymer-1-specific T cells were made by repeated copolymer-1 stimulation of T cells, microglia were isolated from the retinas of newborn rats, and then, they were co-cultured (the experimental group) for 48 h. Retinal ganglion cells were collected from the retinas of adult rats, purified, and then, the supernatants from different groups were added. After 72 h, terminal-deoxynucleotidyl transferase-mediated d-UTP nick end labelling analysis was used to observe retinal ganglion cell apoptosis, and reverse transcription polymerase chain reaction was used to test messenger RNA expression of Caspase-3 and Caspase-8. The levels of cytokines, including insulin-like growth factor-1, brain-derived neurotrophic factor, tumour necrosis factor-α and interleukin-10, in the supernatants were examined by enzyme-linked immunosorbent assay to explore the possible mechanisms undergoing.
  
  
  RESULTS
  After 72 h, the mean retinal ganglion cell apoptosis rate in the experimental group was the lowest (25.36%) among the groups. The messenger RNA expression of Caspase-3 and Caspase-8 in this group was significantly lower than that of the control groups (both P < 0.05). The secretion of interlekin-10 and brain-derived neurotrophic factor, insulin-like growth factor-1 and tumour necrosis factor-α in the supernatant of the experimental group were higher than that of the control groups (both P < 0.05) after co-culture.
  
  
  CONCLUSIONS
  The interaction of copolymer-1-specific T cells with microglia could reduce retinal ganglion cell apoptosis. The related immune mechanisms were complicated. Upregulation of brain-derived neurotrophic factor and insulin-like growth factor-1, and the balance of some pro-inflammatory and anti-inflammatory cytokines may be involved in this protective autoimmunity.
authors.affiliation: Department of Ophthalmology, EENT Hospital of Fudan University, Shanghai, China.
authors.forename: Shaohong
authors.initials: S
authors.lastname: Qian
authors.forename: Yating
authors.initials: Y
authors.lastname: Tang
authors.forename: Lina
authors.initials: L
authors.lastname: Cheng
authors.forename: Xinghuai
authors.initials: X
authors.lastname: Sun
authors.forename: Jie
authors.initials: J
authors.lastname: Tian
authors.forename: Chuandi
authors.initials: C
authors.lastname: Zhou
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology; D015551:Autoimmunity / Q000502:physiology; D002450:Cell Communication / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D018920:Coculture Techniques; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D015870:Gene Expression; D000068717:Glatiramer Acetate; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D020287:In Situ Nick-End Labeling; D008213:Lymphocyte Activation / Q000187:drug effects*; D017628:Microglia / Q000166:cytology*; D008856:Microscopy, Fluorescence; D010455:Peptides / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction; D012165:Retinal Ganglion Cells / Q000166:cytology* / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D016207:Cytokines; D007166:Immunosuppressive Agents; D010455:Peptides; D012333:RNA, Messenger; D000068717:Glatiramer Acetate
keywords: RGC; cop-1-specific T cell; microglia; neuroprotection; protective autoimmunity