Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-2-19
pubmed:abstractText
Mice with targeted deletion of the G protein G(alpha)i2 develop an inflammatory bowel disease closely resembling ulcerative colitis. To better define disease pathogenesis, the mucosal immune system in G(alpha)i2-deficient mice was studied. Phenotypic analysis of large intestine lamina propria lymphocytes revealed a large increase in memory CD4+ T cells (CD44high, CD45RBlow, CD62Llow). Furthermore, expression of the mucosal homing receptor integrin beta7 was increased on mucosal, but not systemic, CD4+ T cells. Analysis of cytokine production revealed a marked increase in proinflammatory Th1-type cytokines in inflamed colons, as compared with wild-type mice or G(alpha)i2-deficient mice without colitis. Thus, IFN-gamma and IL-1beta levels were increased 13-fold and 30-fold, respectively, with more modest increases in IL-6 levels (5-fold) and TNF levels (2-fold). Inflamed colons of G(alpha)i2-deficient mice also demonstrated increased IL-12 p40 mRNA levels. No increase in IL-2, IL-4, IL-5, and IL-10 was seen. Large intestinal epithelial cells in G(alpha)i2-deficient mice with colitis were found by immunohistochemistry to express increased levels of both MHC class I and class II Ags. Colitis was associated with increased IgG levels (60-fold increase), predominantly IgG2a (135-fold increase), in large but not small intestinal secretions. This was shown by ELISPOT analysis to result from local production within the lamina propria.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
158
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1068-77
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9013944-Animals, pubmed-meshheading:9013944-Antibody Formation, pubmed-meshheading:9013944-Antigens, CD, pubmed-meshheading:9013944-Antigens, CD45, pubmed-meshheading:9013944-CD4-Positive T-Lymphocytes, pubmed-meshheading:9013944-Colitis, Ulcerative, pubmed-meshheading:9013944-Cytokines, pubmed-meshheading:9013944-Female, pubmed-meshheading:9013944-GTP-Binding Protein alpha Subunits, Gi-Go, pubmed-meshheading:9013944-Histocompatibility Antigens Class I, pubmed-meshheading:9013944-Histocompatibility Antigens Class II, pubmed-meshheading:9013944-Immunity, Mucosal, pubmed-meshheading:9013944-Immunologic Memory, pubmed-meshheading:9013944-Integrin alpha4, pubmed-meshheading:9013944-Integrin beta Chains, pubmed-meshheading:9013944-Integrins, pubmed-meshheading:9013944-Intestine, Large, pubmed-meshheading:9013944-Intestine, Small, pubmed-meshheading:9013944-L-Selectin, pubmed-meshheading:9013944-Male, pubmed-meshheading:9013944-Mice, pubmed-meshheading:9013944-Mice, Inbred C57BL, pubmed-meshheading:9013944-Mice, Inbred Strains, pubmed-meshheading:9013944-Mice, Knockout, pubmed-meshheading:9013944-T-Lymphocyte Subsets, pubmed-meshheading:9013944-Th1 Cells
pubmed:year
1997
pubmed:articleTitle
G(alpha)i2-deficient mice with colitis exhibit a local increase in memory CD4+ T cells and proinflammatory Th1-type cytokines.
pubmed:affiliation
Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't