Publication: Deficiency of STING Promotes Collagen-Specific Antibody Production and B Cell Survival in Collagen-Induced Arthritis
Issued Date
2020-06-03
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ISSN
16643224
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2-s2.0-85086779900
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Mahidol University
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SCOPUS
Bibliographic Citation
Frontiers in Immunology. Vol.11, (2020)
Suggested Citation
Mookmanee Tansakul, Arthid Thim-uam, Thammakorn Saethang, Jiradej Makjaroen, Benjawan Wongprom, Trairak Pisitkun, Prapaporn Pisitkun Deficiency of STING Promotes Collagen-Specific Antibody Production and B Cell Survival in Collagen-Induced Arthritis. Frontiers in Immunology. Vol.11, (2020). doi:10.3389/fimmu.2020.01101 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/57966
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Title
Deficiency of STING Promotes Collagen-Specific Antibody Production and B Cell Survival in Collagen-Induced Arthritis
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Abstract
© Copyright © 2020 Tansakul, Thim-uam, Saethang, Makjaroen, Wongprom, Pisitkun and Pisitkun. The levels of interferon-alpha are high in the serum and synovial fluid of rheumatoid arthritis (RA) patients. Activation of the stimulator of type I interferon genes (STING) mediates the productions of type I interferon and promotes chronic inflammation. STING plays a significant role in autoimmune lupus mice. However, the function of STING in collagen-induced arthritis (CIA) model has never been described. This study aimed to test the function of STING in CIA. The Sting-deficient mice developed arthritis comparable to WT mice. The levels of anti-collagen antibody from Sting-deficient mice were significantly higher than the WT mice. The B cells derived from Sting-deficient mice showed better survival than WT mice in response to the B cell receptor (BCR) stimulation. Activation of STING also induced B cell death, especially in activated B cells. This study demonstrated that the inhibition of STING promotes anti-collagen antibodies and B cell survival, which suggested that STING acts as a negative regulator of B cell function in the CIA model.