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Author Spotlight: Evaluating Traditional Chinese Therapy for Ankylosing Spondylitis in Mice
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TNF-α Inhibitors Decrease Classical CD14hiCD16- Monocyte Subsets in Highly Active, Conventional Treatment Refractory
Bogdan Batko1, Agata Schramm-Luc2, Dominik S Skiba3,4
1Department of Rheumatology, J. Dietl Specialist Hospital, 31-121 Krakow, Poland. bpbatko@gmail.com.
International Journal of Molecular Sciences
|January 16, 2019
Summary
Tumor necrosis factor-alpha inhibitors (TNFi) alter monocyte subsets in inflammatory arthritis. TNFi treatment decreased classical monocytes and increased nonclassical monocytes, reducing disease activity in ankylosing spondylitis and rheumatoid arthritis.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Monocytes play a critical role in inflammatory joint diseases like ankylosing spondylitis (AS) and rheumatoid arthritis (RA).
- Understanding how treatments affect these immune cells is crucial for managing disease activity.
Purpose of the Study:
- To investigate the impact of tumor necrosis factor-alpha inhibitors (TNFi) on peripheral blood monocyte subpopulations and their activation.
- To compare these effects in patients with active AS and RA who have not previously used TNFi.
Main Methods:
- A 12-week study involving 50 patients (32 AS, 18 RA) with high disease activity, randomized to TNFi or placebo.
- Flow cytometry and clinical assessments were performed at baseline, 4 weeks, and 12 weeks.
Main Results:
- TNFi treatment significantly decreased CD14hiCD16- monocytes and increased CD14dimCD16+ monocytes compared to placebo.
- These monocyte subset shifts were consistent in both AS and RA patients.
- TNFi reduced CD11b and CD11c integrin expression on CD14dimCD16+ monocytes and increased CD45RA+ cell frequency.
Conclusions:
- TNFi therapy induces a shift towards nonclassical monocytes in peripheral blood of AS and RA patients.
- This shift may indicate reduced monocyte recruitment to inflammatory sites, correlating with decreased disease activity.
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