Rheumatoid arthritis bone marrow environment supports Th17 response
PBN-AR
Instytucja
Narodowy Instytut Geriatrii, Reumatologii i Rehabilitacji im. prof. dr hab. med. Eleonory Reicher
Informacje podstawowe
Główny język publikacji
angielski
Czasopismo
ARTHRITIS RESEARCH & THERAPY (40pkt w roku publikacji)
ISSN
1478-6354
EISSN
1478-6362
Wydawca
BIOMED CENTRAL LTD
DOI
URL
Rok publikacji
2017
Numer zeszytu
Strony od-do
1-11
Numer tomu
19
Identyfikator DOI
Liczba arkuszy
0,6
Słowa kluczowe
angielski
Bone marrow
IL-17
IL-15
CCL20
Rheumatoid arthritis
Open access
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Razem z publikacją
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Język
angielski
Treść
Background: Rheumatoid arthritis (RA) is a systemic, autoimmune disease leading to joint destruction and ultimately disability. Bone marrow (BM) is an important compartment in RA, where pathological processes from "outside the joint" can occur. IL-17 is a cytokine that exerts proinflammatory effects and participates in the process of bone destruction. It is believed that IL-17 is involved in pathogenesis of RA. However, little is known about the biology of this cytokine in BM. In the present study we investigated Th17-related cytokines in RA BM. Methods: BM samples were obtained from RA and osteoarthritis (OA) patients during total hip replacement surgery. Levels of IL-17AF, IL-17AA, IL-17FF, IL-1 beta, IL-6, IL-23, TGF-beta and CCL20 in BM plasma were determined by specific enzyme-linked immunosorbent assay tests. Percentage of IL-17-producing cells in BM was evaluated by flow cytometry. The effect of IL-15 stimulation on IL-17 production by BM mononuclear cells was examined in vitro. Results: Increased levels of IL-17AF were observed in BM plasma of RA patients in comparison to OA patients. Increased concentrations of IL-1 beta, IL-6 and CCL20 were observed in RA compared to OA BM plasma. Concordant with these findings, significantly increased percentages of CD3(+) CD4(+) IL-17(+) and CD3(+) CD4(+) IL-17(+) IFN-gamma(+) cells were present in RA BM in comparison to OA BM samples. Finally, abundant in RA BM, IL-15 increased IL-17 production by cultured BM mononuclear cells. Conclusions: In the course of RA, the BM microenvironment can promote the development of Th17 cell responses and overproduction of IL-17AF that may lead to increased inflammation and tissue destruction in RA BM.
Cechy publikacji
review-article
Inne
System-identifier
PX-5a5efe6fd5defae3633fb9e0
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