DPP4 reduces proinflammatory cytokine production in human rheumatoid arthritis synovial fibroblasts
| Autor: | Yuan-Li Huang, Chih-Yang Lin, Wei-Fang Lee, Min-Huan Wu, Chien-Chung Huang, Chin-Jung Hsu, Ju-Fang Liu, Yi-Chin Fong, Chien-Kuo Han, Chih-Hsin Tang, Chun-Hao Tsai |
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| Rok vydání: | 2021 |
| Předmět: |
Physiology
medicine.medical_treatment Dipeptidyl Peptidase 4 Clinical Biochemistry Arthritis Proinflammatory cytokine Arthritis Rheumatoid Immune system Medicine Animals Humans Vildagliptin Inflammation business.industry Synovial Membrane Interleukin Cell Biology Fibroblasts medicine.disease Cytokine Rheumatoid arthritis Sitagliptin Immunology Cytokines business medicine.drug |
| Zdroj: | Journal of cellular physiologyREFERENCES. 236(12) |
| ISSN: | 1097-4652 |
| Popis: | Rheumatoid arthritis (RA) is an autoimmune disorder that is characterized by increasing levels of proinflammatory cytokines. The ubiquitous enzyme dipeptidyl peptidase-4 (DPP4, also known as CD26) regulates different immune disorders, although the effects of DPP4 in RA are uncertain. Here, we found lower levels of DPP4 in RA synovial tissues compared with normal tissues. DPP4 levels were also lower in a rat collagen-induced arthritis model than in control (healthy) rats. Overexpression of DPP4 or exogenous treatment of RA synovial fibroblasts with DPP4 reduced levels of proinflammatory interleukin (IL)-1β, IL-6, and IL-13, and increased anti-inflammatory IL-10 synthesis, while DPP4 inhibitors sitagliptin and vildagliptin increased proinflammatory cytokine production, indicating an enhanced risk of RA development. The evidence suggests that increasing DPP4 expression is a novel strategy for RA disease. |
| Databáze: | OpenAIRE |
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