Activated hepatic stellate cells directly induce pathogenic Th17 cells in chronic hepatitis B virus infection
| Autor: | Lei Li, Jie-min Shi, Jiang Liu, Wei Jiang, Ji-Yao Wang, Yun Liu, Jing Li, Wei-min She |
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| Rok vydání: | 2017 |
| Předmět: |
Adult
Male 0301 basic medicine Hepatitis B virus Interleukin-1beta chemical and pharmacologic phenomena C-C chemokine receptor type 6 Biology Dinoprostone Virus Proinflammatory cytokine Young Adult 03 medical and health sciences Hepatitis B Chronic 0302 clinical medicine RAR-related orphan receptor gamma Hepatic Stellate Cells Humans Cells Cultured Cell Proliferation Interleukin-6 hemic and immune systems Cell Biology Middle Aged Phenotype Coculture Techniques CCL20 030104 developmental biology Cyclooxygenase 2 030220 oncology & carcinogenesis Immunology Hepatic stellate cell Interleukin 12 Th17 Cells Female |
| Zdroj: | Experimental Cell Research. 359:129-137 |
| ISSN: | 0014-4827 |
| Popis: | Th17 cells are involved in liver fibrosis by activating hepatic stellate cells (HSCs). We aimed to investigate whether HSCs are able to regulate the function of Th17 cells and to determine the relevant mechanism. Sixty-five patients diagnosed with chronic hepatitis B (CHB) were enrolled in this study. To determine the effect of HSCs on T cells, naive CD4+T cells and Th17 cells were sorted from CHB patients and cultured with or without activated-HSCs, and cytokine expression and gene transcription were analyzed. In addition, the regulatory mechanism of HSCs was investigated. ELISA and qRT-PCR showed that Th17 cells from CHB patients were more pathogenic, on the basis of the expression of IL-17A, IL-23R, RORC, CCL20 and CCR6, and meanwhile, they could activate the primary HSCs. Co-culture experiments indicated that activated HSCs dramatically promoted proliferation of CD4+T cells in a time- and dose-dependent manner. In addition, they could induce naive CD4+T cells to become Th17 cells which had a more pathogenic phenotype. Moreover, activated HSCs-mediated induction of Th17 cells might depend on the release of IL-1β and IL-6 as well as on the COX-PGE2 pathway. Th17 cells cooperated with HSCs in a proinflammatory feedback loop might provide a better understanding of the pathogenic role of Th17 cells in the chronicity of HBV infection. |
| Databáze: | OpenAIRE |
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