Journal roundup

Abstract

Plasmacytoid dendritic cells (pDCs) accumulate in the CNS during neuroinflammation where they may contribute to immunosurveillance and exert regulatory functions. However, the mechanisms regulating CNS pDC recruitment, together with their functional status and phenotype shortly after they entry into the CNS are poorly understood. In this issue, Garnier et al. demonstrate that circulating pDCs are recruited into the CNS during the acute phase of experimental autoimmune encephalomyelitis (EAE) and maintained numerous pDCspecific phenotypic markers and functional properties, notably their capacity to produce type I IFNs and IL-12 upon stimulation through TLR9. Furthermore, the authors show that blood-derived pDCs solely rely on the expression of CD29 integrins to efficiently enter into the CNS during EAE. Together, this study reinforces the notion that side-effects associated with some disease-modifying drugs in multiple sclerosis, such as natalizumab (anti-VLA-4), might be also linked to their capacity to alter the DC/pDC compartment within the CNS, resulting in alteration of immune surveillance mechanisms.