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大学・研究所にある論文を検索できる 「Clinical Significance of Serum Galectin-9 and Soluble CD155 Levels in Patients with Systemic Sclerosis」の論文概要。リケラボ論文検索は、全国の大学リポジトリにある学位論文・教授論文を一括検索できる論文検索サービスです。

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Clinical Significance of Serum Galectin-9 and Soluble CD155 Levels in Patients with Systemic Sclerosis

千原, 真未 東京慈恵会医科大学 DOI:info:doi/10.1155/2018/9473243

2021.10.22

概要

Signaling through coinhibitory receptors downregulates the immune response to prevent excessive immune activation and maintain optimal immunity and tolerance. The aim of this study was to examine the levels of the soluble forms of coinhibitory receptors and their ligands, namely, galectin-9 (the ligand of T-cell immunoglobulin and mucin domain 3) and CD155 (the ligand of T cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain), and their association with clinical features in patients with systemic sclerosis (SSc). The serum levels of galectin-9 and soluble sCD155 were examined by enzyme-linked immunosorbent assays in patients with SSc, and the results were evaluated with respect to clinical features. Patients with SSc exhibited raised serum levels of galectin-9, but not sCD155. Serum galectin-9 levels were raised not only in patients with diffuse cutaneous SSc but also in patients with limited cutaneous SSc. Furthermore, serum galectin-9 levels correlated positively with the erythrocyte sedimentation rate. In addition, increased serum galectin-9 levels tended to be associated with higher mortality and serious organ involvement. These results suggest that galectin-9, but not CD155, may be involved in the pathogenesis of SSc. In addition, the measurement of serum galectin-9 levels could be used to predict serious organ involvement and high mortality in patients with SSc.

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参考文献

[1] K. Yanaba, “Strategy for treatment of fibrosis in systemic sclerosis: present and future,” The Journal of Dermatology, vol. 43, no. 1, pp. 46–55, 2016.

[2] R. Fleischmajer, J. S. Perlish, and J. R. T. Reeves, “Cellular infil- trates in scleroderma skin,” Arthritis & Rheumatism, vol. 20, no. 4, pp. 975–984, 1977.

[3] A. D. Roumm, T. L. Whiteside, T. A. Medsger, and G. P. Rodnan, “Lymphocytes in the skin of patients with progressive systemic sclerosis. Quantification, subtyping, and clinical cor- relations,” Arthritis & Rheumatism, vol. 27, no. 6, pp. 645–653, 1984.

[4] K. Yanaba, Y. Asano, S. Noda et al., “Increased circulating fibrinogen-like protein 2 in patients with systemic sclerosis,” Clinical Rheumatology, vol. 32, no. 1, pp. 43–47, 2013.

[5] F. A. Schildberg, S. R. Klein, G. J. Freeman, and A. H. Sharpe, “Coinhibitory pathways in the B7-CD28 ligand-receptor fam- ily,” Immunity, vol. 44, no. 5, pp. 955–972, 2016.

[6] K. J. Lafferty and A. J. Cunningham, “A new analysis of alloge- neic interactions,” The Australian Journal of Experimental Biology and Medical Science, vol. 53, no. 1, pp. 27–42, 1975.

[7] A. C. Anderson, N. Joller, and V. K. Kuchroo, “Lag-3, Tim-3, and TIGIT: co-inhibitory receptors with specialized functions in immune regulation,” Immunity, vol. 44, no. 5, pp. 989– 1004, 2016.

[8] A. B. Adams, M. L. Ford, and C. P. Larsen, “Costimulation blockade in autoimmunity and transplantation: the CD28 pathway,” Journal of Immunology, vol. 197, no. 6, pp. 2045– 2050, 2016.

[9] M. Ponsoye, C. Frantz, N. Ruzehaji et al., “Treatment with abatacept prevents experimental dermal fibrosis and induces regression of established inflammation-driven fibrosis,” Annals of the Rheumatic Diseases, vol. 75, no. 12, pp. 2142–2149, 2016.

[10] E. F. Chakravarty, V. Martyanov, D. Fiorentino et al., “Gene expression changes reflect clinical response in a placebo- controlled randomized trial of abatacept in patients with diffuse cutaneous systemic sclerosis,” Arthritis Research & Therapy, vol. 17, no. 1, p. 159, 2015.

[11] S. Sato, M. Fujimoto, M. Hasegawa et al., “Serum soluble CTLA-4 levels are increased in diffuse cutaneous systemic scle- rosis,” Rheumatology (Oxford), vol. 43, no. 10, pp. 1261–1266, 2004.

[12] M. Chiba, K. Yanaba, M. Hayashi, Y. Yoshihara, and H. Nakagawa, “Clinical significance of serum soluble T-cell immunoglobulin and mucin domain 3 levels in systemic scle- rosis: association with disease severity,” The Journal of Derma- tology, vol. 44, no. 2, pp. 194–197, 2017.

[13] K. Yanaba, M. Hayashi, Y. Yoshihara, and H. Nakagawa, “Serum levels of soluble programmed death-1 and pro- grammed death ligand-1 in systemic sclerosis: association with extent of skin sclerosis,” The Journal of Dermatology, vol. 43, no. 8, pp. 954–957, 2016.

[14] F. van den Hoogen, D. Khanna, J. Fransen et al., “2013 classi- fication criteria for systemic sclerosis: an American College of Rheumatology/European League against Rheumatism collabo- rative initiative,” Arthritis & Rheumatism, vol. 65, no. 11, pp. 2737–2747, 2013.

[15] A. T. Masi and Subcommittee For Scleroderma Criteria of the American Rheumatism Association Diagnostic and Therapeu- tic Criteria Committee, “Preliminary criteria for the classifica- tion of systemic sclerosis (scleroderma). Subcommittee for scleroderma criteria of the American rheumatism association diagnostic and therapeutic criteria committee,” Arthritis & Rheumatism, vol. 23, no. 5, pp. 581–590, 1980.

[16] E. C. LeRoy, C. Black, R. Fleischmajer et al., “Scleroderma (systemic sclerosis): classification, subsets and pathogenesis,” The Journal of Rheumatology, vol. 15, no. 2, pp. 202–205, 1988.

[17] S. Sato, H. Ihn, K. Kikuchi, and K. Takehara, “Antihistone antibodies in systemic sclerosis: association with pulmonary fibrosis,” Arthritis & Rheumatism, vol. 37, no. 3, pp. 391– 394, 1994.

[18] V. D. Steen, D. L. Powell, and T. A. Medsger, “Clinical correla- tions and prognosis based on serum autoantibodies in patients with systemic sclerosis,” Arthritis & Rheumatism, vol. 31, no. 2, pp. 196–203, 1988.

[19] K. Yanaba, Y. Asano, K. Akamata et al., “Circulating galectin-1 concentrations in systemic sclerosis: potential contribution to digital vasculopathy,” International Journal of Rheumatic Diseases, vol. 19, no. 6, pp. 622–627, 2016.

[20] P. J. Clements, P. A. Lachenbruch, J. R. Seibold et al., “Skin thickness score in systemic sclerosis: an assessment of interob- server variability in 3 independent studies,” The Journal of Rheumatology, vol. 20, no. 11, pp. 1892–1896, 1993.

[21] R. Saigusa, Y. Asano, K. Nakamura et al., “Systemic sclerosis dermal fibroblasts suppress Th1 cytokine production via galectin-9 overproduction due to Fli1 deficiency,” The Journal of Investigative Dermatology, vol. 137, no. 9, pp. 1850–1859, 2017.

[22] T. Matsushita, M. Hasegawa, Y. Hamaguchi, K. Takehara, and S. Sato, “Longitudinal analysis of serum cytokine concentra- tions in systemic sclerosis: association of interleukin 12 eleva- tion with spontaneous regression of skin sclerosis,” The Journal of Rheumatology, vol. 33, no. 2, pp. 275–284, 2006.

[23] C. Chizzolini, A. M. Dufour, and N. C. Brembilla, “Is there a role for IL-17 in the pathogenesis of systemic sclerosis?,” Immunology Letters, vol. 195, pp. 61–67, 2018.

[24] L. Scussel-Lonzetti, F. Joyal, J. P. Raynauld et al., “Predicting mortality in systemic sclerosis: analysis of a cohort of 309 French Canadian patients with emphasis on features at diag- nosis as predictive factors for survival,” Medicine, vol. 81, no. 2, pp. 154–167, 2002.

[25] C. Bryan, Y. Howard, P. Brennan, C. Black, and A. Silman, “Survival following the onset of scleroderma: results from a retrospective inception cohort study of the UK patient popula- tion,” British Journal of Rheumatology, vol. 35, no. 11, pp. 1122–1126, 1996.

[26] C. Bryan, C. Knight, C. M. Black, and A. J. Silman, “Prediction of five-year survival following presentation with scleroderma: development of a simple model using three disease factors at first visit,” Arthritis & Rheumatism, vol. 42, no. 12, pp. 2660– 2665, 1999.

[27] C. Ferri, G. Valentini, F. Cozzi et al., “Systemic sclerosis: demo- graphic, clinical, and serologic features and survival in 1,012 Italian patients,” Medicine, vol. 81, no. 2, pp. 139–153, 2002.

[28] Y. Allanore, D. Borderie, J. Avouac et al., “High N-terminal pro-brain natriuretic peptide levels and low diffusing capacity for carbon monoxide as independent predictors of the occur- rence of precapillary pulmonary arterial hypertension in patients with systemic sclerosis,” Arthritis & Rheumatism, vol. 58, no. 1, pp. 284–291, 2008.

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