Elevated fibrinogenlike protein 2 in TNBSinduced colitis mice: Association with Th17 and regulatory T cells.
Mol Med Rep
; 16(3): 3445-3454, 2017 Sep.
Article
en En
| MEDLINE
| ID: mdl-28713999
ABSTRACT
The etiology and pathogenesis of inflammatory bowel disease (IBD) is complex and remains to be completely elucidated. Numerous cytokines are associated with the initiation and development of IBD. Fibrinogenlike 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. Therefore, the present study investigated the expression of FGL2 and interleukin (IL)17 in trinitrobenzenesulfonic acid (TNBS)induced colitis mice to identify the function of FGL2, based on the effector CD4+ T helper (Th)17/Treg balance, in IBD. Compared with control mice, TNBSinduced mice exhibited marked alterations in clinical manifestation, including macroscopic and histopathological damage. Intestinal and peripheral expression of FGL2 was upregulated in TNBSinduced mice, while the level of FGL2 in the spleen was decreased. Expression of IL17 in the plasma, colon and spleen was increased in TNBSinduced mice. The percentage of Treg cells was markedly decreased, although Th17 cells were increased following TNBS induction. The results of the present study indicated that, in the colitis model, FGL2 was associated with the immunopathogenesis of IBD.
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Fibrinógeno
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Linfocitos T Reguladores
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Colitis
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Células Th17
Tipo de estudio:
Prognostic_studies
/
Risk_factors_studies
Idioma:
En
Revista:
Mol Med Rep
Año:
2017
Tipo del documento:
Article