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Long-term treatment with anti-alpha 4 integrin antibodies aggravates colitis in G alpha i2-deficient mice.

Bjursten, Malin (författare)
Bland, Paul W (författare)
Willen, Roger, (författare)
Uppsala universitet, Institutionen för genetik och patologi, Uppsala universitet, Institutionen för genetik och patologi
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Hornquist, Elisabeth Hultgren (författare)
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
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Uppsala universitet Medicinska och farmaceutiska vetenskapsområdet. Medicinska fakulteten. Institutionen för genetik och patologi. (creator_code:org_t)
Göteborgs universitet Sahlgrenska akademin. Institutionen för laboratoriemedicin, Avdelningen för klinisk immunologi. 
2005
Engelska.
Ingår i: European journal of immunology. - 0014-2980. ; 35:8, s. 2274-83
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Targeted deletion of the heterotrimeric G protein, Galphai2, in mice induces lethal colitis closely resembling ulcerative colitis. In chronic colitis, migration of circulating leukocytes into the intestinal mucosa is partially dependent on alpha4 integrins. In previous studies, short-term administration of anti-alpha4 integrin antibodies has been shown to attenuate intestinal inflammation, and here we elucidate the effect of long-term administration of anti-alpha4 integrin antibodies on colitis in Galphai2(-/- )mice. Long-term blockade of alpha4 integrin significantly increased the severity of colitis in Galphai2(-/-) mice. The inflammation was confined to the colon, associated with increased cancer in situ, destruction of crypt architecture, and increased production of IL-1beta, TNF-alpha and IFN-gamma. Blockade of alpha4 integrin reduced the recruitment of activated T cells to the small intestine. In strong contrast, there were significantly higher numbers of activated T cells in the colonic lamina propria and epithelium, most probably due to in situ proliferation. Furthermore, treatment with alpha4 integrin antibodies induced decreased levels of total IgA and IgG in sera, whereas total IgM levels were unchanged. These new findings may have implications in the understanding of the progression of chronic intestinal inflammation.

Ämnesord

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

Nyckelord

Animals
Antibodies; Blocking/*adverse effects/therapeutic use
Antibodies; Monoclonal/*adverse effects/therapeutic use
Colitis/*immunology/pathology
Colon/drug effects/immunology
Disease Models; Animal
Female
GTP-Binding Protein alpha Subunit; Gi2
GTP-Binding Protein alpha Subunits; Gi-Go/*deficiency/genetics
Immunoglobulin A/blood
Immunoglobulin G/blood
Inflammatory Bowel Diseases/genetics/immunology/*therapy
Integrin alpha4/*immunology
Lymphoid Tissue/drug effects/immunology
Male
Mice
Mice; Inbred C57BL
Mice; Knockout
Proto-Oncogene Proteins/*deficiency/genetics
Research Support; Non-U.S. Gov't
Spleen/drug effects/immunology
T-Lymphocytes/drug effects/immunology
Time Factors
Antibodies
Blocking
adverse effects
therapeutic use
Antibodies
Monoclonal
adverse effects
therapeutic use
Colitis
immunology
pathology
Colon
drug effects
immunology
Disease Models
Animal
GTP-Binding Protein alpha Subunit
Gi2
GTP-Binding Protein alpha Subunits
Gi-Go
deficiency
genetics
Immunoglobulin A
blood
Immunoglobulin G
blood
Inflammatory Bowel Diseases
genetics
immunology
therapy
Integrin alpha4
immunology
Lymphoid Tissue
drug effects
immunology
Inbred C57BL
Knockout
Proto-Oncogene Proteins
deficiency
genetics
Spleen
drug effects
immunology
T-Lymphocytes
drug effects
immunology

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