Migration of helper T-lymphocyte subsets into inflamed tissues.
The localization of lymphocytes to specific tissues is a finely regulated event that has key implications in the development of chronic allergic inflammation that is associated with allergic rhinitis, atopic dermatitis, and asthma. Key players in the tissue localization of lymphocytes and other allergic effector cells include cellular adhesion molecules and chemokines. The expression or activation pattern of these proinflammatory mediators appears to depend, in part, on the local cytokine milieu. For instance, the T(H)1 phenotype is associated with the upregulation of intercellular adhesion molecule-1 and RANTES, whereas the T(H)2 phenotype is associated with the upregulation of vascular cell adhesion molecule and P-selectin. Notably, the recruitment of certain cell populations, such as eosinophils (hallmark of chronic allergic inflammation), into inflamed tissue sites is dependent on the preferential expression of adhesion molecules, chemokines, and associated receptors. The potential mechanisms that underlie cell migration into inflamed tissue as currently understood are reviewed.
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Department of Pathology, University of Michigan Medical School, Ann Arbor, 48109-0602, USA.
D002465:Cell Movement / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology / Q000473:pathology*; D016176:T-Lymphocyte Subsets / Q000166:cytology*; D018417:Th1 Cells / Q000166:cytology; D018418:Th2 Cells / Q000166:cytology