Dendritic cells (DCs) are recruited to sites of infection where they process antigens and migrate to the draining lymph node in order to trigger specific T cell responses. In the C57BL/6J mouse model of cutaneous Leishmaniasis, monocyte-derived dendritic cells were shown to initiate the protective Th1 response against the parasite. Junctional adhesion molecule C (JAM-C), a tight junction protein expressed on endothelial cells and fibroblasts, was described in the past few years to control leukocyte migration during inflammation. Here we showed that targeting JAM-C with a monoclonal antibody improves the development of cutaneous lesions after Leishmania major infection. Indeed, we observed a two-fold increase in the number of neutrophils and monocyte-derived dendritic cells recruited one-day post infection without affecting the number and function of resident macrophages. In addition, analysis of the draining lymph node populations at several time points after infection showed a higher number of migratory dendritic cells. This enhanced antigen presenting cells recruitment boosted the activation of the Th1 response as shown by the increased number of IFN-γ-producing CD4 T cells. Overall, targeting JAM-C could represent a new way to enhance T cell response in Leishmaniasis as well as other infection diseases.
- Copyright © 2013 by The American Association of Immunologists, Inc.