Requirement of L-selectin for gammadelta T lymphocyte activation and migration during allergic pleurisy: co-relation with eosinophil accumulation.

Intra-thoracic antigenic challenge (ovalbumin, 12.5 microg/cavity) led to increased numbers of gammadelta T lymphocytes in pleural cavities, blood and thoracic lymph nodes in sensitized mice within 48 h. Part of these cells expressed CD62L, which increased on gammadelta T cell surfaces obtained from lymph nodes after ovalbumin (OVA) challenge. Selectin blockade by fucoidan pre-treatment (10 mg/kg, i.v.) impaired in vivo increase in CD25(+) and c-fos(+) gammadelta T cell numbers in lymph nodes, indicating a role for selectins on gammadelta T lymphocyte activation and proliferation. In vivo selectin blockade by fucoidan or alpha-CD62L mAb (200 microg/mice, i.p.) also inhibited OVA-induced gammadelta T cell accumulation in pleural cavities. Confirming the direct effect of CD62L on gammadelta T cell transmigration, the migration of i.v. adoptively-transferred CFSE-labeled gammadelta T lymphocytes into pleural cavities of challenged recipient mice was impaired by fucoidan ex vivo treatment. It is noteworthy that eosinophil influx was also impaired in those mice, indicating that reduced eosinophil migration by CD62L in vivo blockade depended on gammadelta T cell migration via CD62L molecules. Accordingly, pleural gammadelta T lymphocytes from fucoidan-treated mice presented reduced OVA-induced IL-5 and CCL11 production. Supporting these data, the depletion of Vgamma4 T lymphocytes, which are pulmonary gammadelta T cells, decreased OVA-induced eosinophil influx into allergic site. Such results demonstrate that CD62L is crucial for the activation of gammadelta T cells in lymph nodes, for their migration into inflamed tissue and for the modulation of eosinophil influx during allergic response.