Correction: Inhibition of autophagy enhances the antitumor efficacy of T/CAR T cell against neuroblastoma

Following publication of the original article [1], the authors identified an error in the name of one of the authors. The given name and the family name were switched. The correct is presented below: Current author name: Scarsella Marco Correct author name: Marco Scarsella Furthermore, errors were also found in the Fig. 2 of the published version, specifically panel E and panel F. The correct figure is presented below: Incorrect Fig. 2 Autophagy inhibition stimulates MHC-I expression in NB. A) MHC-I levels were determined by flow cytometry in both 9464D and 975A2 cells after Atg7 downregulation by lentiviral infection (shAtg7#2 or shCtrl). Data ± SEM are presented as percentage of positive cells (left) and mean fluorescence intensity (MFI) (right) normalized over shCtrl cells (unpaired Student’s t-test). Each dot represents an independent experiment. Representative immunoblotting shows Atg7 protein levels. Actin was used as a loading control; B-C) MHC-I expression was determined by flow cytometry after treatment with the indicated doses of CQ (B) and SBI-0206965 (C) respectively for 48 h in the 9464D cell line. Data ± SEM are presented as mean fluorescence intensity (MFI) normalized over shCtrl cells (one-way ANOVA followed by Tukey post hoc test); D) MHC-I expression was determined by flow cytometry in a panel of human NB cell lines after treatment with 20 or 40 µM CQ respectively. Data ± SEM are presented as MFI (top) and percentage of positive cells (bottom) normalized over shCTRL cells (one-way ANOVA); E–F) WB analysis of MHC-I protein levels after autophagy inhibition by Bafilomycin A1 (BafA1, 100 nM) or CQ in different human NB cell lines. Representative immunoblotting shows MHC-I expression levels. TUBULIN was used as a loading control. Densitometric analysis of MHC-I expression levels over TUBULIN is shown. Data ± SEM are presented and significance is calculated using two-way ANOVA (*p < 0.05, **p < 0.01; n = 3) Correct Fig. 2 Autophagy inhibition stimulates MHC-I expression in NB. A) MHC-I levels were determined by flow cytometry in both 9464D and 975A2 cells after Atg7 downregulation by lentiviral infection (shAtg7#2 or shCtrl). Data ± SEM are presented as percentage of positive cells (left) and mean fluorescence intensity (MFI) (right) normalized over shCtrl cells (unpaired Student’s t-test). Each dot represents an independent experiment. Representative immunoblotting shows Atg7 protein levels. Actin was used as a loading control; B-C) MHC-I expression was determined by flow cytometry after treatment with the indicated doses of CQ (B) and SBI-0206965 (C) respectively for 48 h in the 9464D cell line. Data ± SEM are presented as mean fluorescence intensity (MFI) normalized over shCtrl cells (one-way ANOVA followed by Tukey post hoc test); D) MHC-I expression was determined by flow cytometry in a panel of human NB cell lines after treatment with 20 or 40 µM CQ respectively. Data ± SEM are presented as MFI (top) and percentage of positive cells (bottom) normalized over shCTRL cells (one-way ANOVA); E–F) WB analysis of MHC-I protein levels after autophagy inhibition by Bafilomycin A1 (BafA1, 100 nM) or CQ in different human NB cell lines. Representative immunoblotting shows MHC-I expression levels. TUBULIN was used as a loading control. Densitometric analysis of MHC-I expression levels over TUBULIN is shown. Data ± SEM are presented and significance is calculated using two-way ANOVA (*p < 0.05, **p < 0.01; n = 3) The correction does not compromise the validity of the conclusions and the overall content of the article. The author group has been updated above and the original article [1] has been corrected.