POS0776 CORRELATION OF PERIPHERAL CD4+GRANZB+CTLS WITH DISEASE SEVERITY IN PATIENTS WITH PRIMARY SJÖGREN’S SYNDROME

Background: Sjogren’s syndrome (SS) is a chronic autoimmune disorder. The major histopathologic lesion of it is a focal lymphocytic infiltrate around ductal and acinar epithelial cells, which include a majority of CD4+T. Several studies have shown that the epithelial cells in SS present diverse phenomena, such as MHC class II overexpression. CD4+T cells with cytotoxic activity (CD4 CTL) have been detected in various immune responses. They are characterized by their ability to secrete perforin and granzyme B to kill the target cells in an MHC class II-restricted fashion. Objectives: So this study was to investigate the correlation of peripheral CD4+GranzB+CTLs with disease severity and organ involvement in patients with primary Sjogren’s syndrome. Methods: We recruited 116 pSS patients and 46 healthy controls using flow cytometry to examine proportion of CD4+GranzB+CTLs in their peripheral blood, and immunofluorescence to test the expression of CD4+GranzB+CTLs in labial gland. The correlations of CD4+GranzB+CTLs and the relevant clinical data were analyzed. Results: We analyzed the percentage of CD4+GranzB+cytotoxic T cells in peripheral blood mononuclear cells (PBMCs) by flow cytometry. Frequency of peripheral CD4+GranzB+CTLs were measured in 116 patients with pSS and 46 healthy controls matched for age and sex. The percentage of CD4+GranzB+CTLs were significantly up-regulated in pSS patients than healthy controls (7.1%±4.9% vs 3.1%±1.9%, p Conclusion: In this study, We provide new evidence indicating involvement of CD4+GranzB+CTLs over activation in the disease pathophysiology of pSS, which may serve as a new biomarker to evaluate the activity and severity of pSS. References: [1]Takeuchi A, Saito T. Front Immunol. (2017) 23:194. [2]Brown DM, et al. Front Immunol. (2016) 9:93. [3]Polihronis M, et al. Clin Exp Immunol. (1998) 114:485-90. [4]Xanthou G, et al. Clin Exp Immunol. (1999) 118:154-63. [5]Maehara T, et al. Ann Rheum Dis. (2017) 76:377-385. [6]Goules AV, et al. Clin Immunol. (2017) 182:30-40. [7]Hashimoto K, et al. Proc Natl Acad Sci U S A. (2019) 116:24242-24251. [8]Croia C, et al. Arthritis Rheumatol. (2014) 66:2545-57. [9]Schmidt D,et al. J Clin Invest. (1996) 97:2027–37. [10]Pandya JM, et al. Arthritis Rheum. (2010) 62:3457–66. [11]Moosig F, et al. Clin Exp Immunol. (1998) 114:113–8. [12]Peeters LM, et al. Front Immunol. (2017) 20:1160. Disclosure of Interests: None declared