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Sökning: onr:"swepub:oai:gup.ub.gu.se/54208" > Transfer of colitis...

Transfer of colitis by Galphai2-deficient T lymphocytes: impact of subpopulations and tissue origin.

Bjursten, Malin, 1976- (författare)
Göteborgs universitet, Institutionen för laboratoriemedicin, Avdelningen för klinisk immunologi, Gothenburg University, Institute of Laboratory Medicine, Dept of Clinical Immunology
Willén, Roger, 1939- (författare)
Hultgren-Hörnquist, Elisabeth, 1965- (författare)
Göteborgs universitet, Institutionen för laboratoriemedicin, Avdelningen för klinisk immunologi, Gothenburg University, Institute of Laboratory Medicine, Dept of Clinical Immunology
Göteborgs universitet Sahlgrenska akademin. Institutionen för laboratoriemedicin, Avdelningen för klinisk immunologi. 
2005
Engelska.
Ingår i: Inflammatory bowel diseases. - 1078-0998. ; 11:11, s. 997-1005
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • To elucidate the potential cell population(s) involved in the induction of colitis in inhibitory G protein Galphai2(-/-) mice, Galphai2-deficient or competent bone marrow or splenic and mesenteric lymph node (MLN) T cells were transferred into immunodeficient mice. The mice were followed up to 23 weeks after transfer, recording changes in body weight. Colitis was graded on hematoxylin and eosin-stained colonic tissue, and production of serum interleukin-18 and colon-derived interferon-gamma was measured using ELISA. After adoptive transfer of Galphai2(-/-) bone marrow, severe colitis developed in irradiated wild type recipients, whereas irradiated Galphai2(-/-) mice increased their life span more than 3 times after transfer of wild type bone marrow, accompanied by significant amelioration of colitis. Neither purified Galphai2(-/-) CD4(+), nor CD8(+) splenic or MLN-derived T cells could induce colitis in recombination-activating gene V(RAG) 2(-/-) recipient mice, whereas transfer of splenic Galphai2(-/-) CD3(+) T cells induced severe colitis. In contrast, transfer of Galphai2(-/-) CD3(+) T cells from the MLN caused only minor histopathological changes in the intestinal mucosa. Finally, serum levels of interleukin-18 and interferon-gamma production from colonic tissue cultures correlated well with disease severity. Our results show that bone marrow transplantation can prolong the life of Galphai2(-/-) mice and ameliorate intestinal inflammation. Splenic CD4(+) or CD8(+) T cells on their own were poor inducers of colitis, whereas the combination of both was highly involved in the induction of intestinal inflammation. Furthermore, we show that the tissue origin of CD3(+) T cells is critical for their potency to induce colitis.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  (hsv//swe)
MEDICAL AND HEALTH SCIENCES  (hsv//eng)

Nyckelord

Animals
Antigens
CD3
Colitis
immunology
physiopathology
Cytokines
blood
Enzyme-Linked Immunosorbent Assay
Female
GTP-Binding Protein alpha Subunit
Gi2
genetics
physiology
Immunocompetence
Lymph Nodes
cytology
Male
Mice
Mice
Knockout
Spleen
cytology
T-Lymphocytes
immunology

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