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Updated: Jul 2, 2026

Generation of Induced-pluripotent Stem Cells Using Fibroblast-like Synoviocytes Isolated from Joints of Rheumatoid Arthritis Patients
Published on: October 16, 2016
TH-17 cells in rheumatoid arthritis
Shiva Shahrara1, Qiquan Huang, Arthur M Mandelin
1Department of Medicine, Feinberg School of Medicine, Northwestern University 240 E Huron, Chicago, IL 60611, USA. s-shahrara@northwestern.edu
T-helper 17 (TH-17) cells are elevated in rheumatoid arthritis (RA) synovial fluid. While interleukin-23 (IL-23) may not drive TH-17 cells in the RA joint, IL-27 and interferon-gamma (IFN-gamma) show potential for therapeutic modulation.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Rheumatoid arthritis (RA) is an autoimmune disease characterized by joint inflammation.
- T-helper 17 (TH-17) cells and their associated cytokines play a significant role in RA pathogenesis.
- Understanding the specific roles of cytokines like IL-23, IL-27, and IFN-gamma in RA is crucial for developing targeted therapies.
Purpose of the Study:
- To quantify TH-17 cells in RA synovial fluid (SF).
- To determine interleukin-17 (IL-17) levels in synovial tissue from RA, osteoarthritis (OA), and normal individuals.
- To examine RA SF macrophages for IL-23, IL-27, and interferon-gamma (IFN-gamma) expression.
Main Methods:
- Flow cytometry was used to determine TH-17 cell abundance in RA SF.
- ELISA quantified IL-17 in synovial tissue and IL-23 in SF.
- Real-time PCR analyzed IL-23, IL-27, and IFN-gamma mRNA levels in SF macrophages.
Main Results:
- TH-17 cells were significantly higher in RA SF compared to peripheral blood.
- RA synovial tissue showed increased IL-17 levels compared to OA and normal tissues.
- RA SF macrophages exhibited increased IL-23, IL-27, and IFN-gamma mRNA expression.
Conclusions:
- TH-17 cells are implicated in RA pathogenesis.
- IL-23 does not appear to be a primary driver of TH-17 cells within the RA joint.
- IL-27 and IFN-gamma represent potential therapeutic targets for modulating TH-17 cells in RA.
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