IK acts as an immunoregulator of inflammatory arthritis by suppressing TH17 cell differentiation and macrophage activation
| Autor: | Jae-Hwan Nam, Seulgi Choi, Jun-Ki Min, Inki Kim, Kyung Won Kang, Sooho Park, Dong Hee Lee, Sang-Myeong Lee, Ha-Na Jung, Su-Jin Moon, Hye-Lim Park |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Multidisciplinary business.industry medicine.drug_class Cellular differentiation Inflammatory arthritis medicine.medical_treatment Inflammation Monoclonal antibody medicine.disease Proinflammatory cytokine 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Cytokine 030220 oncology & carcinogenesis Immunology Medicine Macrophage Synovial fluid medicine.symptom business |
| Zdroj: | SCIENTIFIC REPORTS(7) |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/srep40280 |
| Popis: | Pathogenic T helper cells (TH) and macrophages have been implicated in the development of rheumatoid arthritis (RA), which can lead to severe synovial inflammation and bone destruction. A range of therapies have been widely used for RA, including specific monoclonal antibodies and chemical inhibitors against inflammatory cytokines produced by these cells. However, these have not been sufficient to meet the medical need. Here, we show that in transgenic mice expressing truncated IK (tIK) cytokine, inflammatory arthritis symptoms were ameliorated as the result of suppression of the differentiation of TH1 and TH17 cells and of macrophage activation. During inflammatory responses, tIK cytokine systemically regulated macrophage functions and TH17 cell differentiation through inactivation of the MAPK and NF-κB pathways. Interestingly, the level of tIK cytokine was higher in synovial fluid of RA patients compared with that in osteoarthritis (OA) patients. Our observations suggest that tIK cytokine can counterbalance the induction of inflammatory cells related to RA and thus could be a new therapeutic agent for the treatment of RA. |
| Databáze: | OpenAIRE |
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