Current research status of negative immune checkpoint factors in autoimmune eye diseases_Chinese Journal of Ocular Fundus Diseases

Authors：

Feng Hui ,  Wang Hong

Beijing Ophthalmology & Visual Science Key Laboratory, Beijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China;

Corresponding author：

Wang Hong, Email: wanghongyk@sina.com

Keywords：

Autoimmune eye disease; Immune checkpoint molecules; T cell; Review

DOI：

10.3760/cma.j.cn511434-20230918-00389

Video：

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Autoimmune ocular diseases are a type of inflammatory eye condition characterized by the involvement of the immune response. This includes various types disease such as autoimmune uveitis, thyroid-associated eye disease, and primary Sjögren's syndrome. In recent years, breakthroughs have been achieved in inducing transplant tolerance, understanding tumor immune evasion, and preventing autoimmune diseases using immune checkpoint molecules. Negative immune checkpoints effectively control disease progression by inhibiting T cell proliferation, reducing inflammatory cytokine levels, and ultimately regulating autoimmune balance. Therefore, the negative immune checkpoint molecules are expected to be used as a new therapeutic target in the future, and the combination therapy through the combination of negative immune checkpoint drugs is expected to become an important direction to improve the efficacy of the treatment of autoimmune diseases.

Citation： Feng Hui, Wang Hong. Current research status of negative immune checkpoint factors in autoimmune eye diseases. Chinese Journal of Ocular Fundus Diseases, 2024, 40(5): 402-408. doi: 10.3760/cma.j.cn511434-20230918-00389 Copy

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1. Zou W, Wu Z, Xiang X, et al. The expression and significance of T helper cell subsets and regulatory T cells CD(4)(+) CD(2)(5)(+) in peripheral blood of patients with human leukocyte antigen B27-positive acute anterior uveitis[J]. Graefe's Arch Clin Exp Ophthalmol, 2014, 252(4): 665-672. DOI: 10.1007/s00417-014-2567-9.
2. Zhu Y, Yu Q, Su G, et al. Interferon-alpha2a induces CD4(+) T cell apoptosis and suppresses Th1/Th17 responses via upregulating IRF1-mediated PDL1 expression in dendritic cells from Behcet's uveitis[J/OL]. Clin Immunol, 2023, 250: 109303[2023-04-29]. https://pubmed.ncbi.nlm.nih.gov/36997038/. DOI: 10.1016/j.clim.2023.109303.
3. Sharpe AH. Mechanisms of costimulation[J]. Immunol Rev, 2009, 229(1): 5-11. DOI: 10.1111/j.1600-065X.2009.00784.x.
4. Gilman SC, Noelle RJ. Molecular mechanisms of costimulation[J]. Agents Actions Suppl, 1998, 49: 15-16. DOI: 10.1007/978-3-0348-8857-8_3.
5. Chen L, Flies DB. Molecular mechanisms of T cell co-stimulation and co-inhibition[J]. Nat Rev Immunol, 2013, 13(4): 227-242. DOI: 10.1038/nri3405.
6. Chen Y, Guan SY, Deng J, et al. B7-H3: a promising therapeutic target for autoimmune diseases[J/OL]. Cell Immunol, 2020, 352: 104077[2020-02-21]. https://pubmed.ncbi.nlm.nih.gov/32113615/. DOI: 10.1016/j.cellimm.2020.104077.
7. Wang JY, Wang WP. B7-H4, a promising target for immunotherapy[J/OL]. Cell Immunol, 2020, 347: 104008[2019-11-04]. https://pubmed.ncbi.nlm.nih.gov/31733822/. DOI: 10.1016/j.cellimm.2019.104008.
8. ElTanbouly MA, Zhao Y, Nowak E, et al. VISTA is a checkpoint regulator for naive T cell quiescence and peripheral tolerance[J/OL]. Science, 2020, 367(6475): eaay0524[2020-01-17]. https://pubmed.ncbi.nlm.nih.gov/31949051/. DOI: 10.1126/science.aay0524.
9. Antonioli L, Pacher P, Vizi ES, et al. CD39 and CD73 in immunity and inflammation[J]. Trends Mol Med, 2013, 19(6): 355-367. DOI: 10.1016/j.molmed.2013.03.005.
10. Teft WA, Kirchhof MG, Madrenas J. A molecular perspective of CTLA-4 function[J]. Annu Rev Immunol, 2006, 24: 65-97. DOI: 10.1146/annurev.immunol.24.021605.090535.
11. Pack CD, Bommireddy R, Munoz LE, et al. Tumor membrane-based vaccine immunotherapy in combination with anti-CTLA-4 antibody confers protection against immune checkpoint resistant murine triple-negative breast cancer[J]. Hum Vaccin Immunother, 2020, 16(12): 3184-3193. DOI: 10.1080/21645515.2020.1754691.
12. Blank C, Brown I, Peterson AC, et al. PD-L1/B7H-1 inhibits the effector phase of tumor rejection by T cell receptor (TCR) transgenic CD8+ T cells[J]. Cancer Res, 2004, 64(3): 1140-1145. DOI: 10.1158/0008-5472.can-03-3259.
13. Nikoo M, Rabiee F, Mohebbi H, et al. Nivolumab plus Ipilimumab combination therapy in cancer: current evidence to date[J/OL]. Int Immunopharmacol, 2023, 117: 109881[2023-04-02]. https://pubmed.ncbi.nlm.nih.gov/37012882/. DOI: 10.1016/j.intimp.2023.109881.
14. Klocke K, Holmdahl R, Wing K. CTLA-4 expressed by FOXP3(+) regulatory T cells prevents inflammatory tissue attack and not T-cell priming in arthritis[J]. Immunology, 2017, 152(1): 125-137. DOI: 10.1111/imm.12754.
15. Kubo S, Nakano K, Nakayamada S, et al. Clinical, radiographic and functional efficacy of abatacept in routine care for rheumatoid arthritis patients: Abatacept Leading Trial for RA on Imaging Remission (ALTAIR) study[J]. Clin Exp Rheumatol, 2016, 34(5): 834-841.
16. Lee HJ, Li CW, Hammerstad SS, et al. Immunogenetics of autoimmune thyroid diseases: a comprehensive review[J]. J Autoimmun, 2015, 64: 82-90. DOI: 10.1016/j.jaut.2015.07.009.
17. Chen X, Hu Z, Liu M, et al. Correlation between CTLA-4 and CD40 gene polymorphisms and their interaction in graves' disease in a Chinese Han population[J]. BMC Med Genet, 2018, 19(1): 171. DOI: 10.1186/s12881-018-0665-y.
18. Si X, Zhang X, Tang W, et al. Association between the CTLA-4 +49A/G polymorphism and Graves' disease: a meta-analysis[J]. Exp Ther Med, 2012, 4(3): 538-544. DOI: 10.3892/etm.2012.618.
19. Chen YH, Lightman S, Calder VL. CD4(+) T-Cell plasticity in non-infectious retinal inflammatory disease[J/OL]. Int J Mol Sci, 2021, 22(17): 9584[2021-09-03]. https://pubmed.ncbi.nlm.nih.gov/34502490/. DOI: 10.3390/ijms22179584.
20. Du L, Yang P, Hou S, et al. Association of the CTLA-4 gene with Vogt-Koyanagi-Harada syndrome[J]. Clin Immunol, 2008, 127(1): 43-48. DOI: 10.1016/j.clim.2008.01.004.
21. Zhang J, Zhou P, Hu S, et al. Meta-analysis of the genetic association between PTPN22 and CTLA-4 variants and risk of uveitis[J]. Ophthalmic Res, 2022, 65(3): 264-275. DOI: 10.1159/000521301.
22. Wang S, Shen H, Bai B, et al. Increased CD4(+)CD8(+) double-positive T cell in patients with primary Sjogren's syndrome correlated with disease activity[J/OL]. J Immunol Res, 2021, 2021: 6658324[2021-05-04]. https://pubmed.ncbi.nlm.nih.gov/34095321/. DOI: 10.1155/2021/6658324.
23. Hadj Kacem H, Kaddour N, Adyel FZ, et al. HLA-DQB1 CAR1/CAR2, TNFa IR2/IR4 and CTLA-4 polymorphisms in Tunisian patients with rheumatoid arthritis and Sjogren's syndrome[J]. Rheumatology (Oxford), 2001, 40(12): 1370-1374. DOI: 10.1093/rheumatology/40.12.1370.
24. Gottenberg JE, Loiseau P, Azarian M, et al. CTLA-4 +49A/G and CT60 gene polymorphisms in primary Sjogren syndrome[J]. Arthritis Res Ther, 2007, 9(2): 24. DOI: 10.1186/ar2136.
25. Verwaerde C, Naud MC, Delanoye A, et al. Ocular transfer of retinal glial cells transduced ex vivo with adenovirus expressing viral IL-10 or CTLA4-Ig inhibits experimental autoimmune uveoretinitis[J]. Gene Ther, 2003, 10(23): 1970-1981. DOI: 10.1038/sj.gt.3302101.
26. Goldzweig O, Hashkes PJ. Abatacept in the treatment of polyarticular JIA: development, clinical utility, and place in therapy[J]. Drug Des Devel Ther, 2011, 5: 61-70. DOI: 10.2147/DDDT.S16489.
27. Riley JL. PD-1 signaling in primary T cells[J]. Immunol Rev, 2009, 229(1): 114-125. DOI: 10.1111/j.1600-065X.2009.00767.x.
28. Chen J, Jiang CC, Jin L, et al. Regulation of PD-L1: a novel role of pro-survival signalling in cancer[J]. Ann Oncol, 2016, 27(3): 409-416. DOI: 10.1093/annonc/mdv615.
29. Sun C, Mezzadra R, Schumacher TN. Regulation and function of the PD-L1 checkpoint[J]. Immunity, 2018, 48(3): 434-452. DOI: 10.1016/j.immuni.2018.03.014.
30. Wang Y, Du J, Gao Z, et al. Evolving landscape of PD-L2: bring new light to checkpoint immunotherapy[J]. Br J Cancer, 2023, 128(7): 1196-1207. DOI: 10.1038/s41416-022-02084-y.
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Chinese Journal of Ocular Fundus Diseases

Current research status of negative immune checkpoint factors in autoimmune eye diseases

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