Correction: Corrigendum: Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells

Abstract

Previous work by Képiró et al. describing the photostable blebbistatin derivative para-nitroblebbistatin was inadvertently omitted from the reference list of this Article and should have been cited at instances where this inhibitor is referred to. For example, in the Results section, Képiró et al. should have been cited as follows: 'To test this hypothesis, we used a non-phototoxic form of Blebbistatin (para-nitroblebbistatin), which impairs cell migration ( Supplementary Fig. 2c) and is compatible with GFP imaging (Képiró et al.)'.Képiró, M. et al. para-Nitroblebbistatin, the non-cytotoxic and photostable myosin II inhibitor. Angew. Chem. Int. Ed. Engl. 53, 8211-8215 (2014).

Rab7b regulates dendritic cell migration by linking lysosomes to the actomyosin cytoskeleton

“…3 A). These experiments were performed with bone marrow-derived murine DCs (BMDCs), as previously described ( Bretou et al, 2017 ; Chabaud et al, 2015 ; Vargas et al, 2016 , 2014 ). Similar to human MDDCs, BMDCs were successfully depleted for Rab7b, and the depletion did not affect their maturation ( …”

“…(D) Quantification of mean±s.d. speed fluctuations [calculated as s.d./mean instantaneous speed ( Chabaud et al, 2015 ; Faure-Andre et al, 2008 )]. n >150, three independent experiments.…”

“…While immature DCs are known to change direction frequently, undergoing important speed fluctuations during motion, mature DCs are more persistent ( Chabaud et al, 2015 ; Vargas et al, 2016 ). Interestingly, upon depletion of Rab7b, LPS-DCs still behave like immature DCs, as they have low speed and significantly higher local speed variations compared to control cells, indicating that DCs depleted of Rab7b change direction more frequently while migrating in microchannels ( Fig.…”

“…When encountering danger-associated antigens, for example, microbial products, DCs start a maturation program, where they undergo massive phenotypical and functional changes ( Banchereau et al, 2000 ; Reis e Sousa, 2006 ). In particular, while immature DCs are characterized by a high antigen uptake capacity and a slow intermittent migration mode ( Chabaud et al, 2015 ), mature DCs are less capable of antigen uptake but are highly motile ( Vargas et al, 2016 ). This increase in their migration capacity, together with the upregulation of the CCR7 chemokine receptor at their surface, promotes their migration to lymph nodes for the initiation of adaptive immune responses ( Mellman and Steinman, 2001 ).…”

Maturation of Monocyte-Derived DCs Leads to Increased Cellular Stiffness, Higher Membrane Fluidity, and Changed Lipid Composition

“…Migration is an active process relying on actin and microtubule cytoskeleton remodeling that is accompanied with mechanical cellular changes (49). Pioneer work to address dynamics of the cytoskeleton during DC migration demonstrated that migration is dependent on nonmuscular myosinIIA contractility generating the force for movement of bone marrow-derived DCs in confined microenvironments such as microfabricated channels (50)(51)(52). Further, active remodeling of the actin cytoskeleton and its regulatory proteins is a highly dynamic process including the maturation of DCs, antigen uptake by plasma membrane vesicle internalization to endo-and lysosomal compartments, antigen processing and presentation, recycling of MHC molecules, and DC-T cell interactions at the immunological synapse (48,(53)(54)(55)(56).…”