Eotaxin activates T cells to chemotaxis and adhesion only if induced to express CCR3 by IL-2 together with IL-4

The transmigration and adherence of T lymphocytes through microvascular end othelium are essential events for their recruitment into inflammatory sites . In the present study, we investigated the expression of CC chemokine rece ptor CCR3 on T lymphocytes and the capacities of the CC chemokine eotaxin t o induce chemotaxis and adhesion in T lymphocytes. We have observed a novel phenomenon that IL-2 and IL-4 induce the expression of CCR3 on T lymphocyt es. We also report that CC chemokine eotaxin is a potent chemoattractant fo r IL-2- and IL-4-stimulated T lymphocytes, but not for freshly isolated T l ymphocytes. Eotaxin attracts T lymphocytes via CCR3, documented by the fact that anti-CCR3 mAb blocks eotaxin-mediated T lymphocyte chemotaxis, In com bination with IL-2 and IL-4, eotaxin enhances the expression of adhesion mo lecules such as ICAM-1 and several integrins (CD29, CD49a, and CD49b) on T lymphocytes and thus promotes adhesion and aggregation of T lymphocytes. Th e eotaxin-induced T lymphocyte adhesion could be selectively blocked by a s pecific cAMP-dependent protein kinase inhibitor, H-89, indicating that eota xin activates T lymphocytes via a special cAMP-signaling pathway. Our new f indings all point toward the fact that eotaxin, in association with the Th1 -derived cytokine IL-2 and the Th2-derived cytokine IL-4, is an important T lymphocyte activator, stimulating the directional migration, adhesion, acc umulation, and recruitment of T lymphocytes, and paralleled the accumulatio n of eosinophils and basophils during the process of certain types of infla mmation such as allergy.