Interleukin 17 inhibits progenitor cells in rheumatoid arthritis cartilage

Autor: Burkhard Mai, Sabine Blaschke, Boris Schminke, Sandra Trautmann, Nicolai Miosge
Rok vydání: 2015
Předmět:
0301 basic medicine
Male
Short Communication
Immunology
Inflammation
Core Binding Factor Alpha 1 Subunit
Biology
Antibodies
Monoclonal
Humanized
Proinflammatory cytokine
Arthritis
Rheumatoid
Immunomodulation
03 medical and health sciences
Cartilage Chondrogenesis
Chondrogenic progenitor cells
Rheumatoid arthritis
Interleukin 17 (IL-17)
medicine
Immunology and Allergy
Humans
Progenitor cell
Antibodies
Blocking
Cells
Cultured
Interleukin 3
Aged
Receptors
Interleukin-17
Stem Cells
Interleukin-17
Adalimumab
Antibodies
Monoclonal
Cartilage Chondrogenesis ⋅ Chondrogenic progenitor cells ⋅ Rheumatoid arthritis ⋅ Interleukin 17 (IL‐17)
Middle Aged
Chondrogenesis
3. Good health
030104 developmental biology
Cartilage
Cytokines
Secukinumab
Female
Matrix Metalloproteinase 3
Interleukin 17
Immunotherapy
Stem cell
medicine.symptom
Zdroj: European Journal of Immunology
ISSN: 1521-4141
Popis: Mesenchymal stem cells are known to exert immunomodulatory effects in inflammatory diseases. Immuneregulatory cells lead to progressive joint destruction in rheumatoid arthritis (RA). Proinflammatory cytokines, such as tumour necrosis factor α (TNF-α) and interleukins (ILs) are the main players. Here, we studied progenitor cells from RA cartilage (RA-CPCs) that are positive for IL-17 receptors to determinate the effects of inflammation on their chondrogenic potenial. IL-17A/F reduced the chondrogenic potential of these cells via the upregulation of RUNX2 protein and enhanced IL-6 protein and MMP3 mRNA levels. Blocking antibodies against IL-17 positively influenced their repair potential. Furthermore, treating the RA-CPCs with the anti-human IL-17 antibody secukinumab or the anti-TNF-α antibody adalimumab reduced the proinflammatory IL-6 protein level and positively influenced the secretion of anti-inflammatory IL-10 protein. Additionally, adalimumab and secukinumab in particular reduced RUNX2 protein to promote chondrogenesis. The amelioration of inflammation, particularly via IL-17 antagonism, might be a new therapeutic approach for enhancing intrinsic cartilage repair mechanisms in RA patients. peerReviewed
Databáze: OpenAIRE
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