[From IgE to the cell adhesion molecule].
The aim of this work is to contribute to increasing our knowledge of asthma. The IgE can't alone be imputed in the anaphylactic reaction. Asthma is a bronchial inflammatory disease. The secretion of lymphokines increases the inflammatory response. The eosinophils cells damage the respiratory epithelium. The mast cells and the basophils cells release the chemical mediators and also the cytokines. The adhesion molecules situated in the cell membrane permit leukocyte cells to integrate with extracellular matrix during intra-tissue migration. Adhesion molecules may play a primary role in the pathogenesis of inflammatory response. The key role of the CD4 + T lymphocytes subset appeared in the last years.
Stain
J P
JP
C.H.U. de Rouen.
D001249:Asthma / Q000503:physiopathology*; D001991:Bronchitis / Q000503:physiopathology; D015815:Cell Adhesion Molecules / Q000502:physiology*; D002634:Chemotaxis, Leukocyte; D004804:Eosinophils / Q000378:metabolism; D005109:Extracellular Matrix / Q000502:physiology; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology*; D008222:Lymphokines / Q000502:physiology; D008407:Mast Cells / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology
D015815:Cell Adhesion Molecules; D008222:Lymphokines; D007073:Immunoglobulin E
De l'IgE à la molécule d'adhésion.