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CD4+CD25+ regulatory T cells in irritable bowel syndrome patients.

Artikel i vetenskaplig tidskrift
Författare Nathalie Holmén
Stefan Isaksson
Magnus Simrén
Henrik Sjövall
Lena Öhman
Publicerad i Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
Volym 19
Nummer/häfte 2
Sidor 119-25
ISSN 1350-1925
Publiceringsår 2007
Publicerad vid Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Institutionen för medicin, avdelningen för invärtesmedicin
Sidor 119-25
Språk en
Länkar dx.doi.org/10.1111/j.1365-2982.2006...
Ämnesord Adult, Antigens, CD4, metabolism, Biological Markers, metabolism, Biopsy, Colitis, immunology, pathology, Colon, immunology, pathology, Female, Flow Cytometry, Forkhead Transcription Factors, genetics, Gene Expression, immunology, Humans, Interleukin-2 Receptor alpha Subunit, metabolism, Intestinal Mucosa, immunology, pathology, Irritable Bowel Syndrome, immunology, pathology, Male, Middle Aged, RNA, Messenger, metabolism, T-Lymphocytes, Regulatory, immunology, metabolism
Ämneskategorier Gastroenterologi

Sammanfattning

The aetiology of the irritable bowel syndrome (IBS) is incompletely understood. A low-grade colonic inflammation is frequently seen, but it is unclear to what extent this phenomenon contributes to the pathophysiology of IBS. CD4(+)CD25(+) regulatory T cells (Treg) are implicated to play an important role in suppressing intestinal inflammation. We, therefore, examined whether the intestinal inflammatory process in IBS patients is the result of an altered function and/or frequency of CD25(+) Treg cells. Patients with IBS (n = 34), fulfilling the Rome II criteria, were compared with controls (n = 26). The suppressive activity of blood CD25(+) Treg cells was determined and the frequency of colonic and blood CD25(+) Treg cells was analysed by flow cytometry. The expression of the Treg marker, FOXP3 mRNA, in colonic biopsies was determined by reverse transcription-polymerase chain reaction. Blood CD25(+) Treg cells from IBS patients suppressed the proliferation of blood CD4(+)CD25(low/-) T cells. Similar frequencies of CD25(+) Treg cells were recorded in mucosa and blood of IBS patients and controls. FOXP3 mRNA was equally expressed in the colonic mucosa of patients with IBS and controls. In conclusion, the low-grade intestinal inflammation recorded in patients with IBS is not associated with an altered function or frequency of CD25(+) Treg cells.

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