Cyclooxygenase-1 Regulates the Development of Follicular Th Cells via Prostaglandin E 2

• Published in: The Journal of immunology (1950) 2019-08, Vol.203 (4), p.864
• Main Authors: Liu, Ting, Yang, Qiong, Cao, Ying-Jiao, Yuan, Wei-Ming, Lei, Ai-Hua, Zhou, Pan, Zhou, Wei, Liu, Yong-Dong, Shi, Mao-Hua, Yang, Quan, Tang, Jin-Yi, Wang, Hai-Kun, Zhang, Hui, Yu, Ying, Zhou, Jie
• Format: Article
• Language: English
• Subjects: Animals; Cell Differentiation - immunology; Cyclooxygenase 1 - immunology; Dinoprostone - immunology; Germinal Center - immunology; Lymphocyte Activation - immunology; Mice; Mice, Inbred C57BL; Mice, Knockout; T-Lymphocytes, Helper-Inducer - cytology; T-Lymphocytes, Helper-Inducer - immunology
• ISSN: 1550-6606
• DOI: 10.4049/jimmunol.1801674

Cyclooxygenase (COX)-1, one of the critical enzymes required for the conversion of arachidonic acid to PGs, has been demonstrated to play an important role not only in the cardiovascular system but also in the immune system. COX-1 has been found to regulate early B cell differentiation, germinal center formation, and Ab production of B cells. However, the underlying mechanisms of COX-1-mediated B cell activation remains not fully understood. In this study, we reported that COX-1 is a potential regulator for the development of follicular Th (T ) cells. -deficient ( ) mice displayed a significant reduction of T cells upon influenza infection or immunization with keyhole limpet hemocyanin, which led to a severe impairment of germinal center responses. We further demonstrated that COX-1-derived PGE via binding with its receptors EP2/EP4, represents the underlying mechanism. The administration of EP2/EP4 agonists or PGE almost completely rescued the defective T cell generation in mice. Taken together, our observations indicate that COX-1 plays an important role in the development of T cells.