Altered T lymphocyte response to respiratory syncytial virus in CCR6−/− mice (96.3)

Abstract

Abstract The CC chemokine receptor 6 is unique in the chemokine family because it binds to only a single ligand, CCL20. CCL20 is expressed in epithelial cells in tissues such as skin, gut mucosa and lungs. Studies using CCR6 deficient mice revealed a defect in dendritic cell positioning in the gut mucosa, suggesting a role for CCL20-CCR6 in leukocyte homeostasis and proper positioning of these cells in mucosal tissues. In a mouse model of asthma, CCR6−/− mice showed reduced airway hyperreactivity and less mucus production. The potential pathological role for CCL20-CCR6 led us to investigate this receptor-ligand pair in a mouse model of viral infection caused by respiratory syncytial virus (RSV), a negative strand RNA virus that can cause severe complications in infants, the elderly and immunocompromised individuals. We found that CCR6−/− mice had lower numbers of activated CD4 and CD8 T cells in the lungs at days 6 and 9 post-RSV infection, as well as reduced Th1 and Th2 cytokines in both lungs and lymph nodes. Interestingly, we also found that these mice had more efficiently cleared virus by day 6 post-infection. This suggests the involvement of a cell type other than T lymphocytes that in the absence of CCR6 is able to impart viral immunity. This research is supported by NIH grant AI36302