Mookmanee TansakulArthid Thim-uamThammakorn SaethangJiradej MakjaroenBenjawan WongpromTrairak PisitkunPrapaporn PisitkunChulalongkorn UniversityFaculty of Medicine, Ramathibodi Hospital, Mahidol University2020-08-252020-08-252020-06-03Frontiers in Immunology. Vol.11, (2020)166432242-s2.0-85086779900https://repository.li.mahidol.ac.th/handle/123456789/57966© 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.Mahidol UniversityImmunology and MicrobiologyMedicineArticleSCOPUS10.3389/fimmu.2020.01101