Volume 2 Supplement 3

Abstracts of the 29th Annual Scientific Meeting of the Society for Immunotherapy of Cancer (SITC)

Open Access

Cyclic dinucleotides (CDNs) anti-tumors response by activating DC and NK cell crosstalk

  • Juan Fu1,
  • Drew Pardoll2 and
  • Young J Kim1, 2
Journal for ImmunoTherapy of Cancer20142(Suppl 3):P169

https://doi.org/10.1186/2051-1426-2-S3-P169

Published: 6 November 2014

Intracellular bacterial, Listeria monocytogenes generates cyclic diadenosine monophosphate (c-di-AMP) can active interferon regulatory factor3 (IRF3) and nuclear factor kappa-light-chain-enhancer (NF-κB) and induces B cell and macrophage secretion of IFN-β [1]. Cyclic diguanylic acid (c-di-GMP) also acts as an important signaling molecule in a variety of bacterial species infection functions. IFN-β actives NK cells through Tyk2-STAT1 signal pathway. Our studied showed CDNs anti-tumor effective dependent IFNα/β receptors (IFNAR1/IFNAR2) on the cell plasma membrane. Some study showed c-di-GMP significantly inhibited the proliferation of human colon cancer cells in vitro [2]. Cyclic dinucleotides (CDNs, c-di-AMP and c-di-GMP) are sensed by STING (stimulator of interferon genes). But CDNs were developed for prevent and therapeutic cancers, it was a novel method. We combined GM-CSF-producing tumor vaccine and TLR agonists enhanced systemic anti-tumor immunity. Our studied showed the regimen significantly inhibition mice tumors growth in B16 melanoma and colon cancer in vivo.

Authors’ Affiliations

(1)
Department of Otolaryngology - Head & Neck Surgery, Johns Hopkins University, School of Medicine
(2)
Department of Oncology and the Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, School of Medicine

References

  1. Woodard Joshua, Iavarone Anthony T, Portnoy Daniel A: Science, Vol 328, 25 June, 2010. C-di-AMP secreted by intracellular Listeria monocytogenes activates a host type I interferon response.Google Scholar
  2. Steinberger O, Lapidot Z, Ben-Ishai Z, Amikam D: Elevated expression of the CD4 receptor and cell cycle arrest are induced in Jurkat cells by treatment with the novel cyclic dinucleotide 3', 5'-cyclic diguanylic acid. FEBS Lett. 444 (1999): 125-129.Google Scholar

Copyright

© Fu et al.; licensee BioMed Central Ltd. 2014

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 (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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.

Advertisement