Franck Barrat

1 Introduction Plasmacytoid dendritic cells represent < 1% of peripheral blood mononuclear cells (PBMCs) in humans [1-3]. The most defining feature of pDCs is their capacity to produce high amounts of IFN-I upon sensing of nucleic acids from pathogens, but also from the self [4]. Activated human pDCs also secrete TNF and IL-6, and upregulate co-stimulatory molecules (CD80, CD86, CD40), allowing them to present antigen to T cells and bridge innate sensing with adaptive immune activation [1, 2].

Abstract Glycosylation is central to the localization and function of biomolecules1. We recently discovered that small RNAs undergo N-glycosylation2 at the modified RNA base 3-(3-amino-3-carboxypropyl) uridine (acp3U)3. However, the functional significance of N-glycosylation of RNAs is unknown.

Introduction About 25% of the world's population has been infected with Mycobacterium tuberculosis (Mtb) [1]. Within their lifetime, 5%–10% of latently infected individuals transition into active tuberculosis (TB), which was responsible for ∼1.6 million deaths in 2021 [2]. Patients with active TB display a strong type I IFN (IFN-I)-inducible gene signature compared with people with latent TB infection and healthy controls [3-6].