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MIG in psoriatic arthritis
1Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Abstract:
Monokine induced by interferon (IFN)-γ (MIG) / chemokine (C-X-C motif) ligand 9 (CXCL)9 is involved in the pathogenesis of psoriatic arthritis (PsA). It was demonstrated that both blood plasma-derived dendritic cells (pDCs) and pDCs isolated from rheumatoid arthritis (RA) and PsA synovial fluid (SF), expressed CXC receptor (R) 3 and CXCR4, and that the chemotaxis of blood-derived pDCs is stimulated by MIG, (IFN)-γ-inducible protein 10 (IP-10)/CXCL10, IFN-inducible T-cell α chemoattractant (I-TAC) )/CXCL11 and stromal cell-derived factor 1 (SDF-1)/ CXCL12, present in RA and PsA SF. In PsA patients have been found a Th1 immune predominance at early stage of disease, while a reduction of these chemokines has been observed in long lasting PsA, with a significant increase of monocyte chemoattractant protein-1/IP-10 ratio. This suggest a shift from Th1 to the Th2 immune response in long lasting PsA. High levels of MIG has been found in patients with PsA and autoimmune thyroiditis too. This chemokine has been proposed as a useful marker to monitor the activity as well the progression of PsA. Efforts have been made to modulate or prevent the production of MIG in PsA aiming to alter the course of the disease.
Insights
Monokine induced by interferon-gamma (MIG) plays a role in psoriatic arthritis (PsA) pathogenesis. Elevated MIG levels in PsA patients suggest its potential as a marker for disease activity and progression.
Area of Science:
- Immunology
- Rheumatology
- Molecular Biology
Background:
- Psoriatic arthritis (PsA) pathogenesis involves chemokines like Monokine induced by interferon-gamma (MIG)/CXCL9.
- Plasma-derived dendritic cells (pDCs) express receptors for chemokines found in synovial fluid of Rheumatoid Arthritis (RA) and PsA patients.
Purpose of the Study:
- To investigate the role of MIG and related chemokines in PsA.
- To explore the potential of MIG as a biomarker for PsA activity and progression.
Main Methods:
- Analysis of chemokine and receptor expression in pDCs from blood and synovial fluid.
- Assessment of pDC chemotaxis in response to specific chemokines.
- Evaluation of chemokine levels in PsA patients with varying disease duration.
Main Results:
- pDCs express CXCR3 and CXCR4, and their chemotaxis is stimulated by MIG, CXCL10, CXCL11, and CXCL12 found in RA and PsA synovial fluid.
- Early PsA shows Th1 immune predominance, shifting to Th2 in long-standing disease, indicated by altered chemokine ratios.
- High MIG levels are observed in PsA and autoimmune thyroiditis, suggesting its utility as a monitoring marker.
Conclusions:
- MIG is implicated in PsA pathogenesis and may serve as a valuable biomarker for monitoring disease activity and progression.
- Understanding chemokine dynamics in PsA offers potential therapeutic targets to alter disease course.
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