Immune activation in the small intestine in patients with rheumatoid arthritis
Objectives: To determine whether inflammation in the gut associated immune system is activated in rheumatoid arthritis (RA). The expression of chemokine receptor- (CCR4, CCR5) and cytokine- (interleukin (IL)2, IL10, interferon γ (IFNγ), tumour necrosis factor α (TNFα), and transforming growth factor...
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Published in | Annals of the rheumatic diseases Vol. 63; no. 10; pp. 1327 - 1330 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
BMJ Publishing Group Ltd and European League Against Rheumatism
01.10.2004
BMJ Elsevier Limited |
Subjects | |
Online Access | Get full text |
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Summary: | Objectives: To determine whether inflammation in the gut associated immune system is activated in rheumatoid arthritis (RA). The expression of chemokine receptor- (CCR4, CCR5) and cytokine- (interleukin (IL)2, IL10, interferon γ (IFNγ), tumour necrosis factor α (TNFα), and transforming growth factor β (TGFβ)) specific mRNA in intestinal biopsy samples from patients with RA was examined. Methods: Duodenal biopsy samples from 13 patients with RA and 15 control subjects were studied. The mRNA expression of CCR4, CCR5, IL2, IL10, IFNγ, TNFα, and TGFβ in intestinal biopsy samples was demonstrated by real time quantitative reverse transcriptase-polymerase chain reaction. Results: The mRNA expression of CCR4, CCR5, and IL10 in intestinal biopsy samples was increased in patients with RA in comparison with control subjects (p = 0.001, p = 0.046, p = 0.019). No difference in the expression levels of IL2, IFNγ, TNFα, or TGFβ was seen between patients with RA and controls. Conclusions: The increased intestinal mRNA expression of IL10, CCR5, and CCR4 suggests that gut associated immune cells are activated in patients with RA. |
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Bibliography: | PMID:15361394 href:annrheumdis-63-1327.pdf istex:01CF8837116F65478CFB0F36D4D5232C680EC9C7 local:0631327 Correspondence to: Dr R Nissinen National Public Health Institute, Department of Molecular Medicine, Biomedicum, PO Box 104, 00251 Helsinki, Finland; riikka.nissinen@ktl.fi ark:/67375/NVC-L1HHDPZJ-0 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 0003-4967 1468-2060 1468-2060 |
DOI: | 10.1136/ard.2003.011304 |