Compared with control mice, TNBS‑induced mice exhibited marked alterations in clinical manifestation, including macroscopic and histopathological damage. Therefore, the present study investigated the expression of FGL2 and interleukin (IL)‑17 in trinitro‑benzene‑sulfonic acid (TNBS)‑induced colitis mice to identify the function of FGL2, based on the effector CD4+ T helper (Th)17/Treg balance, in IBD. Fibrinogen‑like protein 2 (FGL2), an immunosuppressive cytokine expressed by regulatory cluster of differentiation (CD)4+ T (Treg) cells, has been identified to be important for immunomodulatory activity in the inflammatory state. Numerous cytokines are associated with the initiation and development of IBD. The etiology and pathogenesis of inflammatory bowel disease (IBD) is complex and remains to be completely elucidated.
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