Lee, K. M., McKimmie, C. S*., Gilchrist, D. S., Pallas, K. J., Nibbs, R. J., Garside, P., McDonald V., Jenkins C., Ransohoff R., Liu L., Milling S., Cerovic V., Graham G.J.
Here we show that the atypical chemokine receptor ACKR2 (D6) acts in vivo to control interactions between stromal lymphatic endothelial cells and inflammatory leukocytes. Without ACKR2, lymphatics can become congested and overloaded with inflammatory leukocytes such as immature dendritic cells and myeloid cells, resulting in edema. Importantly, this results in a reduced migration of dendritic cells from inflamed sites to the draining lymph node, which may have consequences for the proper initiation of adaptive immune responses.
Pictured is a lymphatic vessel (yellow) that lacks ACKR2 expression and consequently becomes decorated with inflammatory immature dendritic cells (red and green)