Linked Life Data

7989777

Source:http://linkedlifedata.com/resource/pubmed/id/7989777

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1995-1-10
pubmed:abstractText
To determine whether the induction of Th2 cell tolerance down-regulates Ag-induced eosinophil recruitment into the tissue, we studied the effect of the in vivo pretreatment with anti-ICAM-1 mAb, anti-LFA-1 mAb, and a soluble Ag on Ag-induced eosinophil infiltration in the trachea of sensitized mice. The in vivo pretreatment with anti-ICAM-1 mAb, anti-LFA-1 mAb, and a soluble Ag inhibited Ag-induced eosinophil infiltration in the mouse trachea in an Ag-specific manner. The pretreatment with anti-LFA-1 mAb and the Ag also had a weak inhibitory effect on the Ag-induced eosinophil infiltration. In contrast, the pretreatment with Ag alone, the combination of anti-ICAM-1 mAb and anti-LFA-1 mAb alone, or the combination of anti-ICAM-1 mAb and the Ag had no significant effect. In addition, the pretreatment with the two mAb and the Ag and, to a lesser degree, the pretreatment with anti-LFA-1 mAb and the Ag also prevented Ag-specific IgE production in mice. In vitro Ag-induced IL-2, IL-4, and IL-5 production was decreased in spleen cells of the mice pretreated with anti-ICAM-1 mAb, anti-LFA-1 mAb, and the Ag, but not with Ag alone or with the combination of anti-ICAM-1 mAb and anti-LFA-1 mAb alone, indicating the induction of both Th1 and Th2 cell tolerance in vivo. These results indicate that the induction of Th2 cell tolerance prevents Ag-induced eosinophil recruitment into the tissue and IgE Ab production and that ICAM-1/LFA-1 interaction is involved as a costimulatory signal in inducing T cell tolerance to a soluble Ag.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
153
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5819-25
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:7989777-Animals, pubmed-meshheading:7989777-Antibodies, Monoclonal, pubmed-meshheading:7989777-Antigens, pubmed-meshheading:7989777-Chemotaxis, Leukocyte, pubmed-meshheading:7989777-Eosinophils, pubmed-meshheading:7989777-Female, pubmed-meshheading:7989777-Immune Tolerance, pubmed-meshheading:7989777-Immunoglobulin E, pubmed-meshheading:7989777-Intercellular Adhesion Molecule-1, pubmed-meshheading:7989777-Interleukin-2, pubmed-meshheading:7989777-Interleukin-4, pubmed-meshheading:7989777-Interleukin-5, pubmed-meshheading:7989777-Interleukins, pubmed-meshheading:7989777-Lymphocyte Function-Associated Antigen-1, pubmed-meshheading:7989777-Mice, pubmed-meshheading:7989777-Mice, Inbred BALB C, pubmed-meshheading:7989777-T-Lymphocytes, pubmed-meshheading:7989777-Th2 Cells, pubmed-meshheading:7989777-Trachea
pubmed:year
1994
pubmed:articleTitle
Induction of T cell tolerance by pretreatment with anti-ICAM-1 and anti-lymphocyte function-associated antigen-1 antibodies prevents antigen-induced eosinophil recruitment into the mouse airways.
pubmed:affiliation
Department of Internal Medicine, Chiba University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't