Chemokines as mediators of allergic inflammation.

The selective distribution of reactive leukocytes to foci of inflammation or lymphoid organs is thought to rely on the generation of highly specific 'attractive' forces which can enhance or subvert the physiological trafficking process. It is becoming increasingly apparent that the selective trafficking of leukocytes is governed by both the release of soluble mediators, or chemoattractants, as well as the matrix upon or through which the cells must traverse. A balance exists between endogenous cellular adhesion receptors (as well as extracellular matrix proteins) and other inducible adhesion receptors which can be up-regulated on this 'docking station'. This dynamic environment provides a prominent signal for leukocyte extravasation from the blood or lymph vessel lumenal surface through to the tissue space. This report reviews current thinking on the delicate interplay between a superfamily of chemoattractant cytokines, the chemokines, and the various classes of cellular adhesion molecules. In it we highlight the idea that the balance between basal and inducible regulators of cell adhesion and migration is critical. Should it be disrupted, the signals responsible for induction and maintenance of an inflammatory response and those responsible for its resolution become disregulated, resulting in inflammatory pathology.