文摘
Intra-thoracic antigenic challenge (ovalbumin, 12.5 µg/cavity) led to increased numbers of γδ 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 γδ 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+ γδ T cell numbers in lymph nodes, indicating a role for selectins on γδ T lymphocyte activation and proliferation. In vivo selectin blockade by fucoidan or α-CD62L mAb (200 µg/mice, i.p.) also inhibited OVA-induced γδ T cell accumulation in pleural cavities. Confirming the direct effect of CD62L on γδ T cell transmigration, the migration of i.v. adoptively-transferred CFSE-labeled γδ 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 γδ T cell migration via CD62L molecules. Accordingly, pleural γδ T lymphocytes from fucoidan-treated mice presented reduced OVA-induced IL-5 and CCL11 production. Supporting these data, the depletion of Vγ4 T lymphocytes, which are pulmonary γδ T cells, decreased OVA-induced eosinophil influx into allergic site. Such results demonstrate that CD62L is crucial for the activation of γδ T cells in lymph nodes, for their migration into inflamed tissue and for the modulation of eosinophil influx during allergic response.