TNF-Α Inhibitors Decrease Classical CD14hiCD16- Monocyte Subsets in Highly Active, Conventional Treatment Refractory Rheumatoid Arthritis and Ankylosing Spondylitis

Autor: Agata Schramm-Luc, Dominik Skiba, Mateusz Siedlinski, Tomasz Mikolajczyk, Bogdan Batko
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Male
0301 basic medicine
rheumatoid arthritis
Lipopolysaccharide Receptors
Arthritis
Rheumatoid
lcsh:Chemistry
0302 clinical medicine
tumor necrosis factor inhibitor
lcsh:QH301-705.5
Spectroscopy
CD11b Antigen
biology
General Medicine
Middle Aged
Computer Science Applications
Treatment Outcome
medicine.anatomical_structure
Integrin alpha M
Rheumatoid arthritis
Female
medicine.symptom
monocytes
Immunosuppressive Agents
Adult
musculoskeletal diseases
CD11c
Inflammation
GPI-Linked Proteins
Placebo
Article
Catalysis
Inorganic Chemistry
03 medical and health sciences
Refractory
ankylosing spondylitis
medicine
Humans
Spondylitis
Ankylosing
Physical and Theoretical Chemistry
Molecular Biology
030203 arthritis & rheumatology
Ankylosing spondylitis
Tumor Necrosis Factor-alpha
business.industry
Monocyte
Receptors
IgG
Organic Chemistry
medicine.disease
Blood Cell Count
CD11c Antigen
030104 developmental biology
lcsh:Biology (General)
lcsh:QD1-999
Immunology
biology.protein
business
disease activity
Zdroj: International Journal of Molecular Sciences, Vol 20, Iss 2, p 291 (2019)
International Journal of Molecular Sciences
Volume 20
Issue 2
ISSN: 1661-6596
Popis: Monocytes are pivotal cells in inflammatory joint diseases. We aimed to determine the effect of TNF-&alpha
inhibitors (TNFi) on peripheral blood monocyte subpopulations and their activation in ankylosing spondylitis (AS) and rheumatoid arthritis (RA) patients with high disease activity. To address this, we studied 50 (32 AS, 18 RA) patients with highly active disease with no prior history of TNFi use who were recruited and assigned to TNFi or placebo treatment for 12 weeks. Cytometric and clinical assessment was determined at baseline, four, and 12 weeks after initiation of TNFi treatment. We observed that treatment with TNFi led to a significant decrease in CD14hiCD16&minus
monocytes in comparison to placebo, while circulating CD14dimCD16+ monocytes significantly increased. The TNFi-induced monocyte subset shifts were similar in RA and AS patients. While the percentage of CD14dimCD16+ monocytes increased, expression of CD11b and CD11c integrins on their surface was significantly reduced by TNFi. Additionally, CD45RA+ cells were more frequent. The shift towards nonclassical CD14dimCD16+ monocytes in peripheral blood due to TNFi treatment was seen in both AS and RA. This may reflect reduced recruitment of these cells to sites of inflammation due to lower inflammatory burden, which is associated with decreased disease activity.
Databáze: OpenAIRE
Externí odkaz: