Role of CCR6 in directing migration of TH17 cells at sites of inflammation or infection

Data has been obtained from our work aiming at defining the role of CCR6 in directing migration of TH17 cells at sites of inflammation or infection. We found that CCR6–deficient (CCR6-KO) mice were resistant to induction of EAE but became susceptible when transferred with small number of CCR6-sufficient T cells. CCR6 was found to be required on a first wave of TH-17 cells that entered the CNS through the choroid plexus epithelial cells, which constitutively expressed CCL20 in both mice and humans. CCR6+ T cells triggered entry of a second wave of T cells that migrated in large numbers into the CNS by crossing activated parenchymal vessels. These results reveal distinct molecular requirements and anatomical sites of lymphocytes entry during development of EAE and suggest that the CCR6-CCL20 axis controls an evolutionary conserved pathway of immune surveillance in the brain.

• molecule type
• chemokine receptor

• cell type
• Th17 cell

• organism type
• Mus musculus,
• Homo sapiens

created over 15 years ago (14 December 2009)    last modified over 12 years ago (17 December 2012)   [ RDF ]   [ RelFinder ]