(1)Journal of the Korean Glaucoma Society
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(9) marked elevations of intraocular pressure (IOP).1,2 Allergic conditions, gastrointestinal diseases, a genetic predisposition, and viruses have been proposed to play roles in PSS pathogenesis.2-6%
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(15) 56. JOURNAL OF THE KOREAN GLAUCOMA SOCIETY. pathogenesis of the disease. In a Japanese case series, HLA4. > Q
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(17) ' Considering 7. 9ROXPH_1XPEHU. of Ophthalmology of St. Vincent’s Hospital, the Catholic University of Korea, from March 2014 to February 2015..
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(30) . antigenic stimulation.. to the tenets of the Declaration of Helsinki. All patients. As a cause of PSS, the herpes viruses have emerged..
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(87) . latency, and reactivation thereof triggers T cell activation.. as determined by clinical assessment. No patient had an. Therefore, chronic CMV infection exhausts the immune. acute systemic or serious concurrent illness; a history of. 11,12. T cell functional dysreg-. ©
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(114) ' . tonometry, and slit-lamp biomicroscopy of the anterior and. cross-sectional study investigated the immune status of pa-. posterior segments of the eye, both at baseline and at each. '. 'X
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(121) . Materials and Methods. at baseline examination.
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(127) . erbation of aqueous humor inflammation in PSS patients, and during cataract surgery in controls. All aqueous humor. Journal of the Korean Glaucoma Society.
(128) 57. JA Choi, et al. : T cell immunity in PS syndrome.
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(172) . kit; LINCO Research, St. Charles, MO, USA) performed. days of aqueous humor sampling. Monoclonal antibodies,. according to the manufacturer’s instructions, and employ-.
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(223) . Table 1. Demographic and clinical characteristics of patients with Posner-Schlossman syndrome and controls. PSS patients (N = 15). Characteristic*. Controls (N = 11). p -value. Demographic characteristics Age (years). 61.2 (11.6). Female (%). 46.1. 63.4 (7.2) 36.4. 0.590† 0.697‡. Ocular characteristics BCVA. 0.63 (0.23) 2. Corneal endothelial cell count (per mm ) Lens status (phakic,%). 2,098.1 (650.2) 83.3. 0.59 (0.32) 2,796.9 (333.2). 0.982† 0.001†. 100.0. 0.055‡. Spherical equivalent (D). -0.6 (1.6). -0.3 (1.9). 0.664†. Baseline IOP (mmHg). 30.7 (19.5). 17.7 (3.2). 0.014†. Maximum IOP (mmHg). 35.8 (14.1). Number of anti-glaucomatics taken. 2.2 (0.8). n/a 0.0 (0.0). <0.001†. PSS = Posner-Schlossmann syndrome; BCVA = best-corrected visual acuity; IOP = intraocular pressure; n/a = not applicable. * ª
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(235) 58. JOURNAL OF THE KOREAN GLAUCOMA SOCIETY.
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(244) . 9ROXPH_1XPEHU. Results. 15.6–1,000.0 pg/mL. \
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(260) ¤'¡Q'% ' . ©> '=X&ª='. number of PSS patients requiring anti-glaucoma eyedrops. Table 2. Laboratory data on Posner-Schlossman syndrome patients and controls. PSS patients (N = 15). Controls (N = 11). p -value. 6,100 (170). 7,400 (230). 0.148†. Neutrophil (%). 56.9 (11.2). 57.7 (8.6). 0.857†. Lymphocyte (%). 31.2 (8.1). 33.2 (8.1). 0.552†. Monocyte (%). 8.0 (2.9). 7.0 (1.4). 0.274†. Eosinophil (%). 3.4 (3.2). 1.9 (1.4). 0.181†. Basophil (%). 0.6 (0.3). 0.5 (0.2). 0.302†. RBC count (106/μL). 4.2 (0.4). 4.5 (0.3). 0.086†. Hemoglobin (g/dL). 13.1 (1.4). 14.0 (1.5). 0.178†. 228.6 (63.0). 228.7 (41.7). 0.996†. 0.26 (0.42). 0.07 (0.04). 0.176†. 6.6 (2.3). 8.0 (0.0). 0.119†. 168.4 (73.8). 0.303†. Characteristic* Complete blood count WBC count (cells/μL). Platelet count (103/μL) C-reactive protein (mg/L) Immunology HSV IgG titer (AU/mL) CMV IgG titer (AU/mL). 208.2 (55.8). PSS = Posner-Schlossmann syndrome; WBC = white blood cell; RBC = Red Blood cell; HSV = herpes simplex virus; CMV = cytomegalovirus. *. ª
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(269) U-test.. Figure 1. Absolute blood cell counts of Pos-. Seg. Lympho. Monocyte. Eosinophil. Basophil. ner-Schlossman syndrome (PSS) patients and controls. Patients with PSS had a significantly lower absolute lymphocyte count (1,931 ± 325 cells/mm3) than the control group (2,328 ± 507 cell/mm3; p = 0.041). Seg = segmented neutrophil; Lympho = lymphocyte. Journal of the Korean Glaucoma Society.
(270) JA Choi, et al. : T cell immunity in PS syndrome. A. B. C. D. E. F. 59. Figure 2. lymphocyte subpopulations (numbers of cells/mm3) in Posner-Schlossman syndrome (PSS) patients and controls. The PSS and. control groups differed significantly in T-cell subpopulation numbers; these were generally lower in the PSS group, particularly the numbers of CD4+ (A) and CD8+ T cells (B), (p = 0.058 and 0.029, respectively) In the PSS group, the CD8+CD28- (D) and CD8+CD57+ T cell numbers (E), indicating immunosenescence were also lower than in the control group, but the differences were marginally significant (p = 0.085 and 0.085, respectively).. !\'\¡^'
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(294) . cells/mm ; p = 0.041) (Fig. 1). No patient had HSV or CMV. immunological status of PSS patients. To the best of our. DNA in the aqueous humor..
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(330) 60. JOURNAL OF THE KOREAN GLAUCOMA SOCIETY. 9ROXPH_1XPEHU. A. B. C. D. E. F. Figure 3 . Cytokine levels of Posner-Schlossman syndrome (PSS) patients and controls. The TGF-¹1 were significantly lower in the PSS group than in the control group (D),(p = 0.012) IL-2 and the TGF-¹2 tended to be lower in the PSS than the control group with marginal significance (E). TGF = transforming growth factor; IL = interleukin; IFN = interferon; PD-L = Programmed Death- ligand 1.. PSS patients did not exhibit T cell immunosenescence,.
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(343) !p = 0.041, Fig.. et al.18 found that PSS patients had elevated aqueous humor chemokine levels, compared to controls.. 1). Relative peripheral blood lymphopenia has several caus-. The cause of systemic T cell activation in PSS patients. es, such as recent infection, corticosteroid use, malnutrition,. remains unclear. None of our patients had CMV or HSV. rheumatic disease, severe stress, intense physical exercise,. DNA in their aqueous humor samples, although all patients. 15,16. The most common cause of. '%
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(382) JA Choi, et al. : T cell immunity in PS syndrome. Uniquely, the anterior chamber exhibits strong immunosup-. 61. immunity in PSS patients.. pressive features, particularly in the context of cellular im
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(408) . receptor. PD-L1 is the ligand of the Programmed Death-1. Helsinki.. (PD-1) receptor, and the PD-1/PD-L1 complex sends an
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(442) ing surgery.9 Our study had certain limitations. First, the aqueous hu
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(467) . www.koreanglaucoma.org. References 1. Posner A, Schlossman A. Syndrome of unilateral recurrent
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(472) 1948;39:517-35. \'
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(474) #
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(478) comatocyclitic crisis. Semin Ophthalmol 2011;26:282-4. 3. Knox DL. Glaucomatocyclitic crises and systemic disease: peptic ulcer, other gastrointestinal disorders, allergy and stress. Trans Am Ophthalmol Soc 1988;86:473-95. Q' %
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(480) %'%#=> Q
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(483) tocyclitic crisis. Arch Ophthalmol 1985;103:1837-9. 5. Chee SP, Bacsal K, Jap A, et al. Clinical features of cytomegalovirus anterior uveitis in immunocompetent patients. Am J Ophthalmol. 2008;145:834-40. 6. Jap A, Chee SP. Viral anterior uveitis. Curr Opin Ophthalmol 2011;22:483-8. '
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(486) !ford) 2010;49:621-31..
(487) 62. JOURNAL OF THE KOREAN GLAUCOMA SOCIETY. 9ROXPH_1XPEHU. 8. Woo JH, Lim WK, Ho SL, Teoh SC. Characteristics of cy-. 18. Li J, Ang M, Cheung CM, et al. Aqueous cytokine. tomegalovirus uveitis in immunocompetent patients. Ocul.
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(495) ' # . 9. Su CC, Hu FR, Wang TH, et al. Clinical outcomes in. 2012;7:e44453.. cytomegalovirus-positive Posner-Schlossman syndrome. 19. Ohno S. Immunological aspects of Behçet’s and Vogt-.
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(500) '= $. Koyanagi-Harada’s diseases. Trans Ophthalmol Soc U K. Ophthalmol 2014;158:1024-31.e2.. 1981;101(Pt 3):335-41.. 10. Chee SP, Jap A. Presumed fuchs heterochromic iridocycli-. \^'
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(509) '%#= . tis and Posner-Schlossman syndrome: comparison of cyto-. $
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(514) . megalovirus-positive and negative eyes. Am J Ophthalmol 2008;146:883-9.e1.. 1977;26:591-5. \' >¸
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(516) ' %#= >\ . 11. Fletcher JM, Vukmanovic-Stejic M, Dunne PJ, et al. Cyto-.
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(523) . keratoplasties for herpetic corneal scars. Ophthalmologe. continuously driven to replicative exhaustion. J Immunol 2005;175:8218-25. \'
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(530) munosenescence: from basics to clinics. Immun Ageing 2012;9:23.. 2007;104:705-8. 22. Streilein JW. Ocular immune privilege: therapeutic opportunities from an experiment of nature. Nat Rev Immunol 2003;3:879-89. \¤' &
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(548) #¦. ease. Immunology 2011;134:17-32.. cell lines. Cytokine 2011;56:231-8.. 14. Smithey MJ, Li G, Venturi V, et al. Lifelong persistent vi-. 24. Zhang JY, Zhang Z, Jin B, et al. Cutting edge: programmed. ral infection alters the naive T cell pool, impairing CD8 T. death-1 up-regulation is involved in the attrition of cyto-. cell immunity in late life. J Immunol 2012;189:5356-66..
(549) ¦
(550) . 15. Ng WL, Chu CM, Wu AK, et al. Lymphopenia at pre-. hepatitis B virus infection. J Immunol 2008;181:3741-4..
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(559) ' º$. cell programming by cytomegalovirus stunts naive T. 2006;99:37-47..
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(562) ' $ . 16. Hedfors E, Holm G, Pettersson D. Lymphocyte subpopulations in sarcoidosis. Clin Exp Immunol 1974;17:219-26.. 2008;180:4836-47. 26. Hsu PN, Yang TC, Kao JT, et al. Increased PD-1 and. ' = £ %
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