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Correction to: Determinant roles of dendritic cell-expressed Notch Delta-like and Jagged ligands on anti-tumor T-cell immunity

  • 1,
  • 1,
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  • 2, 4, 11, 12Email author and
  • 1Email author
Contributed equally
Journal for ImmunoTherapy of Cancer20197:124

https://doi.org/10.1186/s40425-019-0592-2

  • Received: 9 April 2019
  • Accepted: 9 April 2019
  • Published:

The original article was published in Journal for ImmunoTherapy of Cancer 2019 7:95

Correction to: J Immunother (2019) 7:95

https://doi.org/10.1186/s40425-019-0566-4

Following publication of the original article [1], the author reported the wrong version of Figs. 5 and 7 have been published. The correct version of the figures can be found below:
Fig. 5
Fig. 5

Monomeric soluble DLL1 or Dll1-ablated dendritic cells restrict Notch signaling and impair T-cell cytotoxic responses. a Expression of Notch downstream target Hes1 mRNA was assessed by qRT-PCR in 3 T3 cells treated with clustered DLL1 in the presence of soluble DLL1 (sDLL1) construct at indicated concentrations for 16 h. b, c T-cell proliferation was measured after co-incubating allogeneic T-cells labeled with Cell Tracer Violet fluorescent dye with bone marrow-derived Dll1−/− or wild-type DC in the presence of soluble anti-CD3 for 5 days. In some T-cell cultures with wild-type DC, soluble DLL1 construct was added at the indicated concentrations. Representative Cell Tracer Violet dye dilution profile is shown (b). d Tumor volume was measured in LLC tumor-bearing mice treated with sDLL1 construct 1 mg/kg body weight, i.p. every 2 days for 20 days. e IFN-γ producing tumor-infiltrating cells from these mice were enumerated by ELISPOT assay on day 18 after LLC tumor initiation. Mean ± SEM, 8 mice per group; *, p < 0.05; **, p < 0.005. f, g C57BL/6 mice were transplanted with BALB/c heart allografts on day 0 and treated with sDLL1 construct (1 mg/kg) i.p. on days − 3, − 1, 1, 3, 5 and 7. f Heart allografted C57BL/6 mice log-rank survival. g IFN-γ ELISPOT assay on recipient CD8+T cells isolated after heart allograft and re-stimulated with mitomycin C-treated donor spleen cells in the presence of recipient C57BL/6 splenocytes. h Percentage of FoxP3+ cells among CD4+ splenocytes after heart allograft. Mean ± SEM, 4–8 mice per group; *, p < 0.05

Fig. 7
Fig. 7

Dendritic cell Jagged expression correlates with PD-1 expression on T-effector-memory cells. a Purified T cells were stimulated in vitro in a T:DC (3:1) stimulation co-culture with allogeneic bone marrow-derived dendritic cells in the presence of CD3/CD28 beads (1 μg/mL) for four days with or without treatment with clustered DLL1 (1.5 μg/mL) or monovalent soluble JAG1 (20 μg/mL) constructs. Expression of CD62L, CD44, CTLA-4 and PD-1 was assessed on gated populations as indicated by flow cytometry. Dot plots from a representative experiment out of two independent experiments with duplicates are shown. b-c Lung tumor single cell suspensions from 10 patients were evaluated for the expression of NOTCH ligands on tissue-resident CD11b+CD11chigh dendritic cells and PD-1 and NOTCH receptors in populations of T cells by flow cytometry. NOTCH ligands in CD11b+CD11chigh cells were compared to PD-1 positivity of Tem and Tcm cells (b) or to NOTCH receptor positive T cell subsets by Pearson’s correlation (c). All p-values were corrected using the Benjamani- Hochberg procedure; n = 8; * p < 0.05. Color code indicates the strength of correlation. d Scheme summarizing available data on the regulation of T cell responses by Notch ligands

The original article has been corrected as well.

Notes

Declarations

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Division of Medical Oncology, Department of Internal Medicine, The Ohio State University Wexner Medical Center and The James Comprehensive Cancer Center, 460 W 12th Ave, 484 BRT, Columbus, OH 43210, USA
(2)
Department of Biochemistry, Cancer Biology, Neuroscience and Pharmacology, Meharry Medical College School of Medicine, 2005 Harold D. West Basic Sciences Building, 1023 21st Ave N, Nashville, TN 37208, USA
(3)
Department of Microbiology, Immunology and Physiology, Meharry Medical College School of Medicine, Nashville, USA
(4)
School of Graduate Studies and Research, Meharry Medical College, Nashville, TN, USA
(5)
Sechenov First Moscow State Medical University, Moscow, Russia
(6)
Division of Hematology, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA
(7)
Department of Chemistry and Biochemistry, The Ohio State University, Columbus, OH, USA
(8)
Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, USA
(9)
Department of Pathology, West Virginia University, Morgantown, WV, USA
(10)
Department of Medicine, Vanderbilt University, Nashville, TN, USA
(11)
Host–Tumor Interactions Research Program, Vanderbilt-Ingram Comprehensive Cancer Center, Vanderbilt University, Nashville, TN, USA
(12)
Vanderbilt Institute for Infection, Immunology and Inflammation, Vanderbilt University, Nashville, TN, USA

Reference

  1. Tchekneva, et al. J ImmunoTherapy Cancer. 2019;7:95. https://doi.org/10.1186/s40425-019-0566-4.View ArticleGoogle Scholar

Copyright

© The Author(s). 2019

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