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  • Poster presentation
  • Open Access

Core skin DC signatures control immune tolerance to skin cancer and limit anti-tumor immunity

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Journal for ImmunoTherapy of Cancer20153 (Suppl 2) :P205

  • Published:


  • Melanoma
  • Dendritic Cell
  • Skin Cancer
  • Melanoma Skin
  • Clonal Proliferation


Dendritic cells (DC) are gatekeepers of immunity, critical to both an initiate immune response upon infection and promote tolerance to self-antigens.


We have just established that DC subsets in the skin that constitutively migrate into LNs can individually and collectively temper an on-going immune response. Tissue DC originating in skin share a unique transcriptome signature geared towards immune dampening when compared to their lymphoid counterparts in both mouse and human.


Here we demonstrate expression of unique core skin DC transcripts are closely associated with increased clinical aggressiveness of BCC in humans and the stratify stage 4 melanoma outcomes. In mice, loss of signature genes in DC, which include but are not limited to PD-L1/PD-L2, lead to enhanced antigen-specific immunity, decreased tumor growth, and improved anti-tumor vaccine priming to melanoma skin cancer by distinguishable molecular control of T cell effector function and clonal proliferation.


These data suggest core skin DC signatures regulate the immune-epithelial interface.

Authors’ Affiliations

Brigham and Women's Hospital, Department of Dermatology, Harvard Medical School, Boston, MA, USA
Stanford University, Stanford, CA, USA
Mount Sinai school of Medicine, New York, NY, USA
Harvard Medical School, Boston, MA, USA


© Nirschl et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.