Study on the correlation between chemotactic factor CXCL11 and its receptor CXCR7 with disease activity in systemic lupus erythematosus#br#
ZU Beibei1 CHEN Yanhong2 RAO Yongmei3 LI Meirong3 LIU Lin3 MA Qianqian3▲
1.Xuzhou Institute of Medical Science, Jiangsu Province, Xuzhou 221009, China;
2.Department of Laboratory Medicine, Xuzhou Central Hospital, Jiangsu Province, Xuzhou 221009, China;
3.Department of Rheumatology and Immunology, Xuzhou Central Hospital, Jiangsu Province, Xuzhou 221009, China
Abstract:Objective To investigate the correlation of CXC-type chemotactic factor (CXC) ligand 11 and its receptor CXCR7 with disease activity in systemic lupus erythematosus (SLE). Methods The enrolled 40 SLE patients were the first onset patients from October 2018 to October 2020 in the Department of Rheumatology and Immunology of Xuzhou Central Hospital of Jiangsu Province (hereinafter referred to as “our hospital”). According to the SLE disease activity index, they were divided into SLE non-disease activity group (10 cases), mild disease activity group (10 cases), moderate-severe disease activity group (20 cases); a total of 20 healthy subjects in our hospital during the same period were selected as the control group. Enzyme-linked immunosorbent assay and flow cytometry were used to detect the expressions of CXCL11, CD3+CXCR7+ T cells, and CD19+CXCR7+ B cells in peripheral blood of SLE patient group and healthy control group, respectively, while the relationship between CXCL11, CXCR7 and SLE disease activity were analyzed. Results The expression levels of CD3+CXCR7+T cells, CD19+CXCR7+B cells, and CXCL11 in peripheral blood of the SLE group were higher than those of the healthy control group, and the differences were highly statistically significant (P < 0.01). There were significant differences in the levels of CD19+CXCR7+, CD3+CXCR7+, and CXCL11 in SLE patients in different disease activity groups (P < 0.05). Among them, the indicators in the inactive disease group, the mild activity group, and the moderately severe activity group were higher than those in the healthy control group, while the indicators of the mild activity group and the moderate to severe activity group were higher than those of the inactive disease group, the indexes in the moderate-severe activity group were higher than those in the mild activity group, and the differences were statistically significant (P < 0.05). The expressions of CD3+CXCR7+T cells, CD19+CXCR7+B cells, and CXCL11 in SLE patients were positively correlated with systemic lupus erythematosus disease activity index score, dsDNA, erythrocyte sedimentation rate, and C-reactive protein (r > 0, P < 0.05); negatively correlated with complement C3 (r < 0, P < 0.05). Conclusion CXCL11 and CXCR7 are not only highly expressed in SLE patients, but may also be involved in the occurrence, development and disease activity of SLE. Chemokines CXCL11 and CXCR7 can be used as indicators of SLE disease activity.
祖蓓蓓1 陈艳红2 饶咏梅3 李美荣3 刘琳3 马倩倩3▲. 趋化因子CXCL11及其受体CXCR7与系统性红斑狼疮疾病活动相关性研究[J]. 中国医药导报, 2022, 19(13): 96-98,103.
ZU Beibei1 CHEN Yanhong2 RAO Yongmei3 LI Meirong3 LIU Lin3 MA Qianqian3▲. Study on the correlation between chemotactic factor CXCL11 and its receptor CXCR7 with disease activity in systemic lupus erythematosus#br#. 中国医药导报, 2022, 19(13): 96-98,103.
[1] Arriens C,Wren JD,Munroe ME,et al. Systemic lupus erythematosus biomarkers: the challenging quest [J]. Rheumatology (Oxford),2017,56(suppl_1): i32-i45.
[2] Aringer M,Petri M. New classification criteria for systemic lupus erythematosus [J]. Curr Opin Rheumatol,2020,32(6):590-596.
[3] Laufer JM,Legler DF. Beyond migration-chemokines in lymphocyte priming,differentiation,and modulating effector functions [J]. J Leukoc Biol,2018,104(2):301-312.
[4] Lounsbury N. Advances in CXCR7 Modulators [J]. Pharmaceuticals (Basel),2020,13(2):33-48.
[5] Nguyen HT,Reyes-Alcaraz A,Yong HJ,et al. CXCR:a β-arrestin-biased receptor that potentiates cell migration and recruits β-arrestin2 exclusively through Gβγ subunits and GRK2 [J]. Cell Biosci,2020,10(1):134-153.
[6] Tawalbeh SM,Marin W,Morgan GA,et al. Serum protein biomarkers for juvenile dermatomyositis:a pilot study [J]. BMC Rheumatol,2020,10(4):52-67.
[7] Puchert M,Koch C,Zieger K,et al. Identification of CXCL11 as part of chemokine network controlling skeletal muscle development [J]. Cell Tissue Res,2021,384(2):499-511.
[8] Elia G. MIG in psoriatic arthritis [J]. Clin Ter,2018, 169(6):e297-e302.
[9] Crescioli C,Corinaldesi C,Riccieri V,et al. Association of circulating CXCL10 and CXCL11 with systemic sclerosis [J]. Ann Rheum Dis,2018,77(12):1845-1846.
[10] Watanabe K,Penfold ME,Matsuda A,et al. Pathogenic role of CXCR7 in rheumatoid arthritis [J]. Arthritis Rheum,2010,62(11):3211-3220.
[11] Padern G,Duflos C,Ferreira R,et al. Identification of a Novel Serum Proteomic Signature for Primary Sj?觟gren’s Syndrome [J]. Front Immunol,2021,23(12)1-12.
[12] Yang P,Tan J,Yuan Z,et al. Expression profile of cytokines and chemokines in osteoarthritis patients: Proinflammatory roles for CXCL8 and CXCL11 to chondrocytes [J]. Int Immunopharmacol,2016,40(11):16-23.
[13] Bombardier C,Gladman DD,Urowitz MB,et al. Derivation of the SLEDAI. A disease activity index for lupus patients. The Committee on Prognosis Studies in SLE [J]. Arthritis Rheum,1992,35(6):630-640.
[14] Hochberg MC. Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus [J]. Arthritis Rheum,1997,40(9):1725-1734.
[15] Vacchini A,Locati M,Borroni EM. Overview and potential unifying themes of the atypical chemokine receptor family [J]. J Leukoc Biol,2016,99(6):883-892.
[16] Hughes CE,Nibbs RJB. A guide to chemokines and their receptors [J]. FEBS J,2018,285(16):2944-2971.
[17] Laufer JM,Legler DF. Beyond migration-chemokines in lymphocyte priming,differentiation,and modulating effector functions [J]. J Leukoc Biol,2018,104(2):301-312.
[18] Ulvmar MH,Hub E,Rot A. Atypical chemokine receptors [J]. Exp Cell Res,2011,317(5):556-568.
[19] Steen A,Larsen O,Thiele S,et al. Biased and g protein-independent signaling of chemokine receptors [J]. Front Immunol,2014,5(277):1-7.
[20] Wang C,Chen W,Shen J. [J]. Front Pharmacol,2018,21(9):641-649.
[21] Nibbs RJ,Graham GJ. Immune regulation by atypical chemokine receptors [J]. Nat Rev Immunol,2013,13(11):815-829.
[22] Singh AK,Arya RK,Trivedi AK,et al. Chemokine receptor trio:CXCR3,CXCR4 and CXCR7 crosstalk via CXCL11 and CXCL12 [J]. Cytokine Growth Factor,2013,24(1):41-49.
[23] Wedemeyer MJ,Mahn SA,Getschman AE,et al. The chemokine X-factor:Structure-function analysis of the CXC motif at CXCR4 and ACKR3 [J]. J Biol Chem,2020,295(40):13927-13939.
[24] Oda K,Kotani T,Takeuchi T,et al. Chemokine profiles of interstitial pneumonia in patients with dermatomyositis: a case control study [J]. Sci Rep,2017,7(1):1635-1645.
[25] Zhou J,Yu Q. Disruption of CXCR3 function impedes the development of Sjogren’s syndrome-like xerostomia in non-obese diabetic mice [J]. Lab Invest,2018,98(5):620-628.