Down-regulation of activated T and Th17/IL-22 producing CD4+ T cells with treatment in Kawasaki disease

Jingying Yang, Guanfang Liu, Maohua Zhou, Juan Cheng, Erxia Shen, Xiaoqiong Gu, Hairui Xie

Abstract


Abstract: Kawasaki disease (KD) has emerged as one of the most common causes of pediatric acquired heart disease in developed countries. T cell abnormal activation is involved in the pathogenesis of KD. IVIG plus aspirin treatment is the first line for KD. Given that the responses of CD4+ T and CD8+ T cells after this treatment in the KD patients remain poorly understood, the present study aimed to determine and compare the frequency, activation and function of CD4+ T and CD8+ T cells before and after IVIG plus aspirin treatment in the KD patients using flow cytometry. The results showed that the most significant differences noted between before and after treatment were the reduced percentage of CD69+ CD4+ T cells, as well as the decreased frequency of Th17 cells and IL-22+ CD4+ T cells after IVIG treatment. Furthermore, IVIG plus aspirin treatment could not change the frequency of IFN-γ+CD8+ T cells in the peripheral blood from the patients with KD, although CD69+CD8+ T cells were decreased. The down-regulation of activated T and Th17/IL-22 producing CD4+T cells after treatment in KD implies the role of Th17 cells and IL-22+ CD4+ T cells in the pathogenesis of KD.


Keywords


Kawasaki disease, IVIG, CD4+ T, Th17, CD8+ T

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References


Kawasaki, T., [Acute febrile mucocutaneous syndrome with lymphoid involvement with specific desquamation of the fingers and toes in children]. Arerugi, 1967. 16(3): p. 178-222.

Cohen, E. and R. Sundel, Kawasaki Disease at 50 Years. JAMA Pediatr, 2016. 170(11): p. 1093-1099.

Chen, S., et al., Coronary Artery Complication in Kawasaki Disease and the Importance of Early Intervention. JAMA Pediatrics, 2016. 170(12): p. 1156.

Selamet Tierney, E.S., et al., Vascular Health in Kawasaki Disease. Journal of the American College of Cardiology, 2013. 62(12): p. 1114-1121.

Uehara, R. and E.D. Belay, Epidemiology of Kawasaki Disease in Asia, Europe, and the United States. Journal of Epidemiology, 2012. 22(2): p. 79-85.

Greco, A., et al., Kawasaki disease: An evolving paradigm. Autoimmunity Reviews, 2015. 14(8): p. 703-709.

Jane W. Newburger, M.M.M.T., Kawasaki Disease. Journal of the American College of Cardiology, 2016. 67(14): p. 1738-1749.

Guo, M.M., et al., Th17- and Treg-related cytokine and mRNA expression are associated with acute and resolving Kawasaki disease. Allergy, 2015. 70(3): p. 310-8.

Galeotti, C., et al., Predisposing factors, pathogenesis and therapeutic intervention of Kawasaki disease. Drug Discovery Today, 2016. 21(11): p. 1850-1857.

Galeotti, C., et al., Kawasaki disease: Aetiopathogenesis and therapeutic utility of intravenous immunoglobulin. Autoimmunity Reviews, 2010. 9(6): p. 441-448.

Weyand, C.M. and J.J. Goronzy, Immune mechanisms in medium and large-vessel vasculitis. Nat Rev Rheumatol, 2013. 9(12): p. 731-40.

Takahashi, K., T. Oharaseki and Y. Yokouchi, Update on etio and immunopathogenesis of Kawasaki disease. Current Opinion in Rheumatology, 2014. 26(1): p. 31-36.

Jia, S., et al., The T helper type 17/regulatory T cell imbalance in patients with acute Kawasaki disease. Clinical & Experimental Immunology, 2010. 162(1): p. 131-137.

Noval Rivas, M., et al., CD8+ T Cells Contribute to the Development of Coronary Arteritis in theLactobacillus casei Cell Wall Extract-Induced Murine Model of Kawasaki Disease. Arthritis & Rheumatology, 2017. 69(2): p. 410-421.

Ye, Q., et al., Intravenous immunoglobulin treatment responsiveness depends on the degree of CD8 + T cell activation in Kawasaki disease. Clinical Immunology, 2016. 171: p. 25-31.

Rowley, A.H., et al., The transcriptional profile of coronary arteritis in Kawasaki disease. BMC Genomics, 2015. 16: p. 1076.

Newburger, J.W., et al., Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Statement for Health Professionals From the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. PEDIATRICS, 2004. 114(6): p. 1708-1733.

Newburger, J.W., Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Statement for Health Professionals From the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation, 2004. 110(17): p. 2747-2771.

Vani, J., et al., Role of natural antibodies in immune homeostasis: IVIg perspective. Autoimmunity Reviews, 2008. 7(6): p. 440-444.

Dhanrajani, A. and R.S.M. Yeung, Revisiting the role of steroids and aspirin in the management of acute Kawasaki disease. Current Opinion in Rheumatology, 2017. 29(5): p. 547-552.

Lo, M.S. and J.W. Newburger, Role of intravenous immunoglobulin in the treatment of Kawasaki disease. Int J Rheum Dis, 2018. 21(1): p. 64-69.

Ding, Y., et al., Profiles of responses of immunological factors to different subtypes of Kawasaki disease. BMC Musculoskelet Disord, 2015. 16: p. 315.

Rowley, A.H., et al., Allograft Inflammatory Factor-1 Links T-Cell Activation, Interferon Response, and Macrophage Activation in Chronic Kawasaki Disease Arteritis. Journal of the Pediatric Infectious Diseases Society, 2017. 6(3): p. e94-e102.

Ehara, H., et al., Early activation does not translate into effector differentiation of peripheral CD8T cells during the acute phase of Kawasaki disease. Cellular Immunology, 2010. 265(1): p. 57-64.

Rasouli, M., B. Heidari and M. Kalani, Downregulation of Th17 cells and the related cytokines with treatment in Kawasaki disease. Immunology Letters, 2014. 162(1): p. 269-275.

Infante-Duarte, C., et al., Microbial Lipopeptides Induce the Production of IL-17 in Th Cells. The Journal of Immunology, 2000. 165(11): p. 6107-6115.

Torchinsky, M.B. and J.M. Blander, T helper 17 cells: discovery, function, and physiological trigger. Cellular and Molecular Life Sciences, 2010. 67(9): p. 1407-1421.

Li, S., et al., Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments. Mediators of Inflammation, 2014. 2014: p. 1-10.

Maddur, M.S., et al., Inhibition of differentiation, amplification, and function of human TH17 cells by intravenous immunoglobulin. Journal of Allergy and Clinical Immunology, 2011. 127(3): p. 823-830.e7.

Hsieh, K.S., et al., Treatment of Acute Kawasaki Disease: Aspirin's Role in the Febrile Stage Revisited. PEDIATRICS, 2004. 114(6): p. e689-e693.




DOI: http://dx.doi.org/10.15383/jbt.2018001

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