Lymphocyte traffic control by chemokines

In contrast to the remarkable chemokine responses of phagocytes and monocyt es that were documented early on, lymphocytes have been considered for a lo ng time to be poor targets for chemokine action. This view has changed dram atically with the discovery that peripheral blood T cells need to be activa ted before they can migrate in response to inflammatory chemokines. These c hemokines do not act on the bulk of resting T cells that are in circulation . The identification of a new group of chemokines that selects resting, as opposed to effector, T and B cells was very exciting. These inflammation-un related chemokines affect transendothelial migration and localization of pr ogenitor and mature lymphocytes in lymphoid and nonlymphoid tissues. Here, we summarize the current view of chemokine-mediated lymphocyte traffic and focus on the molecular mechanisms by which T cell responses to chemokines a re modulated. Recent developments in this area justify the hypothesis that the distinct migration patterns of lymphocytes throughout their life cycle- that is, during lymphopoiesis, antigen-dependent priming, inflammation and immune surveillance-are finely tuned by changing sets of chemokines that ar e selective for developmentally regulated chemokine receptors. Thus, the ch emokine system assures that cell traffic during inflammatory responses occu rs in the proper spatial and temporal fashion and disturbance of this syste m, therefore, can lead to inflammatory disease.