Basic studies on uveitis in China have progressed rapidly in recent years. First， a series of studies have demonstrated that several molecules （such as Tim-3 and IDO） and regulatory T cells （such as CD4+CD25+， CD4+PD-1+， CD8+Foxp3+ and CD8+CD94+T cells） are involved in the development of anterior chamber-associated immune deviation （ACAID）. Secondly， immunological studies reveal that both Th1 and Th17 cells are involved in the pathogenesis of uveitis. Increased resistance of lymphocytes to apoptosis， and the decreased frequencies and functioning of CD4+CD25+ T cells are involved in the development or recurrence of uveitis. Thirdly， a number of genes have been shown to be associated with Behcet′s disease or Vogt-Koyanagi-Harada syndrome in Chinese patients. In addition， using an animal model of experimental autoimmune uveitis （EAU）， interferon-β and interleukins have been demonstrated to be involved in the development of EAU. Mesenchymal stem cells ameliorate the immune responses in EAU. However， it is worthwhile to pointing out that there are only a few researchers performing basic research on uveitis in China and that the mechanisms involved in this disease should be further investigated in the future.
杨培增,杜利平. 我国葡萄膜炎基础研究的现状[J]. 中华眼视光学与视觉科学杂志, 2015, 17(5): 257-260.
Yang Peizeng,Du Liping. Basic studies on uveitis in China. Chinese Journal of Optometry Ophthalmology and Visual science, 2015, 17(5): 257-260. DOI: 10.3760/cma.j.issn.1674-845X.2015.05.001
Wang Y， Yang P， Li B， et al. Expression of Tim-3 is transiently increased before development of anterior chamber-associated immune deviation[J]. Ocul Immunol Inflamm，2006，14（3）：151-156.
[3]
Meng Q， Yang P， Li B， et al. CD4（+）PD-1（+） T cells acting as regulatory cells during the induction of anterior chamber-associated immune deviation[J]. Invest Ophthalmol Vis Sci，2006，47（10）：4444-4452.
[4]
Zhang HN， Yang PZ， Zhou HY， et al. Involvement of Foxp3-expressing CD4（+） CD25（+） regulatory T cells in the development of tolerance induced by transforming growth factor-beta（2）-treated antigen-presenting cells[J]. Immunology，2008，124（3）：304-314.
[5]
Li B， Yang P， Zhou H， et al. Upregulation of T-bet expression in peripheral blood mononuclear cells during Vogt-Koyanagi-Harada disease[J]. Br J Ophthalmol，2005，89（11）：1410-1412.
[6]
Chi W， Yang P， Li B， et al. IL-23 promotes CD4+ T cells to produce IL-17 in Vogt-Koyanagi-Harada disease[J]. J Allergy Clin Immunol，2007，119（5）：1218-1224.
[7]
Chi W， Zhu X， Yang P， et al. Upregulated IL-23 and IL-17 in Behcet patients with active uveitis[J]. Invest Ophthalmol Vis Sci，2008，49（7）：3058-3064.
[8]
Amadi-Obi A， Yu CR， Liu X， et al. TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1[J]. Nat Med，2007，13（6）：711-718.
[9]
Ye Z， Wang C， Tang J， et al. Decreased interleukin-37 expression in vogt-koyanagi-harada disease and upregulation following immunosuppressive treatment[J]. J Interferon Cytokine Res，2015，35（4）：265-272.
[10]
Wang C， Tian Y， Ye Z， et al. Decreased interleukin 27 expression is associated with active uveitis in Behcet′s disease[J]. Arthritis Res Ther，2014，16（3）：R117.
[11]
Xu M， Wang C， Tian Y， et al. Inhibition of proinflammatory cytokine by IL-25 in Vogt-Koyanagi-Harada syndrome[J]. Ocul Immunol Inflamm，2014，22（4）：294-299.
[12]
Cai T， Wang Q， Zhou Q， et al. Increased expression of IL-22 is associated with disease activity in Behcet′s disease[J]. PLoS One，2013，8（3）：e59009.
[13]
Yang Y， Du L， Sun M， et al. IFN-beta inhibits the increased expression of IL-9 during experimental autoimmune uveoretinitis[J]. PLoS One，2012，7（10）：e48566.
[14]
Xiang Q， Chen L， Hou S， et al. TRAF5 and TRAF3IP2 gene polymorphisms are associated with Behcet′s disease and Vogt-Koyanagi-Harada syndrome： a case-control study[J]. PLoS One，2014，9（1）：e84214.
[15]
Hou S， Du L， Lei B， et al. Genome-wide association analysis of Vogt-Koyanagi-Harada syndrome identifies two new susceptibility loci at 1p31.2 and 10q21.3[J]. Nat Genet，2014， 46（9）：1007-1011.
[16]
Qi J， Hou S， Zhang Q， et al. A functional variant of pre-miRNA-196a2 confers risk for Behcet′s disease but not for Vogt-Koyanagi-Harada syndrome or AAU in ankylosing spondylitis[J]. Hum Genet，2013，132（12）：1395-1404.
[17]
Hou S， Qi J， Zhang Q， et al. Genetic variants in the JAK1 gene confer higher risk of Behcet′s disease with ocular involvement in Han Chinese[J]. Hum Genet，2013，132（9）：1049-1058.
[18]
Du LP， Yang PZ， Hou SP， et al. Association of the CTLA-4 gene with Vogt-Koyanagi-Harada syndrome[J]. Clini Immunol，2008，127（1）：43-48.
[19]
Zhou Q， Hou S， Liang L， et al. MicroRNA-146a and Ets-1 gene polymorphisms in ocular Behcet's disease and Vogt-Koyanagi-Harada syndrome[J]. Ann Rheum Dis，2014，73（1）：170-176.
[20]
Jiang Z， Yang P， Hou S， et al. IL-23R gene confers susceptibility to Behcet's disease in a Chinese Han population[J]. Ann Rheum Dis，2010，69（7）：1325-1328.
[21]
Sun M， Yang Y， Yang P， et al. Regulatory effects of IFN-beta on the development of experimental autoimmune uveoretinitis in B10RIII mice[J]. PLoS One，2011，6（5）：e19870.
[22]
Chen S， Yan H， Sun B， et al. Subretinal transfection of chitosan-loaded TLR3-siRNA for the treatment of experimental autoimmune uveitis[J]. Eur J Pharm Biopharm，2013，85（3 Pt A）：726-735.
[23]
Fang CB， Zhou DX， Zhan SX， et al. Amelioration of experimental autoimmune uveitis by leflunomide in Lewis rats[J]. PLoS One，2013，8（4）：e62071.
[24]
Li G， Yuan L， Ren X， et al. The effect of mesenchymal stem cells on dynamic changes of T cell subsets in experimental autoimmune uveoretinitis[J]. Clin Exp Immunol，2013，173（1）：28-37.
[25]
Song J， Bi H， Xie X， et al. Preparation and evaluation of sinomenine hydrochloride in situ gel for uveitis treatment[J]. Int Immunopharmacol，2013，17（1）：99-107.
[26]
Zhang X， Wang J， Xu Z， et al. The impact of rhubarb polysaccharides on Toll-like receptor 4-mediated activation of macrophages[J]. Int Immunopharmacol，2013，17（4）：1116-1119.
浙公网安备 33030202001892号