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Updated: Jul 12, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
The expression of SOCS is altered in rheumatoid arthritis
P Isomäki1, T Alanärä, P Isohanni
1Department of Molecular Immunology, Institute of Medical Technology, Biokatu 8, 33014 Tampere University, Tampere, Finland. pia.isomaki@uta.fi
Objectives:
Cytokines play a key pathogenic role in rheumatoid arthritis (RA). Several cytokines signal through the JAK-STAT pathway, which is negatively regulated by the suppressors of cytokine signalling (SOCS) proteins. Since SOCS protein levels can profoundly modulate cellular responses to cytokines, we have investigated their expression in chronic RA.
Methods:
The levels of SOCS1-3 and CIS1 mRNA in peripheral blood (PB) and synovial fluid (SF) mononuclear cells (MCs), purified T cells and monocytes from RA patients and healthy volunteers were studied using quantitative reverse transcriptase polymerase chain reaction (RT-PCR). SOCS mRNA and protein expression in synovial tissues were examined by RT-PCR and immunohistochemistry.
Results:
The levels of SOCS1 and SOCS3 were significantly increased in PBMCs from RA patients when compared with healthy volunteers. These differences were mainly due to up-regulation of SOCS1 in PB T cells and of SOCS3 in PB monocytes. In addition, SOCS2 was up-regulated in PB T cells. Interestingly, SF T cells expressed lower and SF macrophages higher levels of SOCS molecules than their PB counterparts. Similarly, while a significant portion of macrophages in synovial tissues expressed SOCS1 and SOCS3 proteins, the majority of T cells remained SOCS negative. Finally, SOCS1 was up-regulated in the synovial membranes from patients with RA when compared with osteoarthritis.
Conclusions:
SOCS expression levels are profoundly altered in RA, and the profile of SOCS expression is dependent on both the cell type as well as the cellular compartment.
Insights
Suppressors of cytokine signalling (SOCS) protein expression is altered in rheumatoid arthritis (RA) patients. SOCS levels vary by cell type and location, impacting cellular responses to cytokines in RA.
Area of Science:
- Immunology
- Molecular Biology
- Rheumatology
Background:
- Cytokines are key drivers of rheumatoid arthritis (RA) pathogenesis.
- The JAK-STAT pathway, crucial for cytokine signaling, is regulated by suppressors of cytokine signalling (SOCS) proteins.
- SOCS protein levels significantly influence cellular responses to cytokines.
Purpose of the Study:
- To investigate the expression patterns of SOCS proteins in chronic RA.
- To determine if SOCS expression differs between RA patients and healthy individuals.
- To explore cell-type and compartment-specific differences in SOCS expression within RA.
Main Methods:
- Quantitative reverse transcriptase polymerase chain reaction (RT-PCR) was used to measure SOCS1-3 and CIS1 mRNA levels.
- Peripheral blood (PB) and synovial fluid (SF) mononuclear cells, including purified T cells and monocytes, were analyzed.
- Immunohistochemistry was employed to examine SOCS mRNA and protein expression in synovial tissues.
Main Results:
- SOCS1 and SOCS3 mRNA levels were significantly elevated in PBMCs of RA patients compared to healthy volunteers.
- Up-regulation of SOCS1 was observed in PB T cells, while SOCS3 was up-regulated in PB monocytes.
- SF T cells showed lower SOCS expression, whereas SF macrophages exhibited higher levels compared to their PB counterparts. SOCS1 was also elevated in RA synovial membranes versus osteoarthritis.
Conclusions:
- SOCS expression profiles are significantly altered in rheumatoid arthritis.
- The observed changes in SOCS expression are dependent on specific cell types.
- Cellular compartment (e.g., peripheral blood vs. synovial fluid) also dictates SOCS expression patterns in RA.
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