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Mouse Models for Graft Arteriosclerosis

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Investigating the Role of Type I Interferon Signaling on Muscle Disease Using Mouse Models.

Rita Spathis¹, Sabrina Narvesen¹, Deeva Robles Kuriplach¹

¹Department of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, Binghamton University, Binghamton, New York.

Arthritis & Rheumatology (Hoboken, N.J.)

|February 18, 2026

Summary

Tofacitinib improved survival and reduced the type I interferon (IFN) signature in myositis mouse models. Type I IFN signaling drives muscle inflammation and weakness, highlighting its therapeutic potential.

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Area of Science:

Immunology
Rheumatology
Pharmacology

Background:

Dysregulated type I interferon (IFN) signaling is implicated in the pathogenesis of autoimmune myositis.
Understanding the role of type I IFNs in muscle vasculature and identifying effective therapeutic targets are crucial.

Purpose of the Study:

To investigate the therapeutic efficacy of Janus kinase (JAK) inhibitors, specifically baricitinib and tofacitinib, in mouse models of myositis.
To examine the impact of type I IFNs on muscle vasculature and inflammation.

Main Methods:

Myositis was induced in MHC class I transgenic (HT) mice, followed by treatment with baricitinib, tofacitinib, or vehicle.
Survival, weight, muscle strength, histopathology, and IFN-stimulated gene expression were assessed.
A separate model involved IFNβ overexpression in C57BL/6 mice treated with tofacitinib to evaluate its effects on muscle inflammation and function.

Main Results:

Tofacitinib significantly reduced IFN scores in myositis mice and improved survival rates compared to vehicle and baricitinib groups.
IFNβ overexpression led to increased muscle inflammation, reduced grip strength, and elevated IFN and H2Kb expression.
Baricitinib did not show significant benefits in reducing IFN scores or improving survival in the myositis model.

Conclusions:

Tofacitinib demonstrates therapeutic potential by mitigating the type I IFN signature and improving survival in myositis models.
Type I IFN signaling is a key contributor to muscle inflammation and weakness, reinforcing its role as a therapeutic target.
Further research is warranted to explore the functional recovery aspects and precise mechanisms of JAK inhibitors in myositis.