Adhesion Molecules in Leukocyte Endothelial Interaction
Neutrophils are the front line defense against most microbial pathogens. They provide a rapid, relatively nonspecific defense mechanism, after which a more long lasting, antigen-specific response is established by T and B lymphocytes. To fulfill this role successfully, the neutrophil must be able to migrate from the blood into the area of inflammation, a process which involves activation of endothelial cells and leukocyte by inflammatory stimuli, adherence to the endothelial surface at the site of inflammation, and migration through endothelium to extravascular tissue. The orchestration of these steps must by precisely regulated to ensure a rapid response to isolate and destroy the invading pathogen yet cause minimal damage to healthy tissues (Etzioni and Douglas 1993). The process of leukocyte accumulation at sites of inflammation is a dynamic one, involves multiple steps and is mediated by several families of adhesion molecules (Springer 1995). These include the Integrins, the Selectins and members of the Immunoglobulin (Ig) superfamily. Each is involved in a different phase of leukocyte emigration through the endothelium and the synchronization of their expression and function is crucial for the normal recruitment of leukocyte from the blood stream to the tissue (Etzioni 1996).
KeywordsMigration Arthritis Carbohydrate Codon Recombination
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- Anderson DC, Kishimoto TK, Smith CW. 1995 Leukocyte adhesion deficiency and other disorders of leukocyte adherence and motility. In: Scriver CR, Beaudet AL, Sly WS, Valle D. Eds: The metabolic and molecular bases of inherited diseaes. 7th Ed. McGraw-Hill, New-York pp3955–95.Google Scholar
- Etzioni A, Douglas DS. 1993 Microbial phagocytosis and killing in host defense. In Spirer Z, Roifman CM, Branski D.Eds: Pediatric Immunology. Karger, Basel pp 17–27.Google Scholar
- Kishimoto TK, Rothlein R 1993 Adhesion molecules which guide neutrophil endothelial cell interaction at site of inflammation. In: Gupta S, Griscelli C, eds. New concepts in immunodeficiency diseases. New York, John Wiley & Sons. 131–52.Google Scholar