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Kwon and Koh: Resistance to Chemotherapy on Tumor Through Cathepsin B-dependent Activation of the NLRP3 Inflammasome
Letter to the Editor

J Bacteriol Virol 2013;43(3):233-234.

Published online: 9 February 2013

DOI: https://doi.org/10.4167/jbv.2013.43.3.233

Resistance to Chemotherapy on Tumor Through Cathepsin B-dependent Activation of the NLRP3 Inflammasome

Eun-Jeong Kwon, Young-Sang Koh*

Jeju National University School of Medicine, Jeju, Korea

*Corresponding author: Young-Sang Koh. Department of Microbiology & Immunology, Jeju National University School of Medicine, 102 Jejudaehakno, Jeju 690-756, Korea. Phone: +82-64-754-3851, Fax: +82-64-702-2687, e-mail: yskoh7@jejunu.ac.kr

Received 25 July 201330 July 2013       Accepted 1 August 2013

Copyright © 2013 Journal of Bacteriology and Virology

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Anticancer drugs kill tumor cells and increase host anti-tumor immunity. Interestingly, gemcitabin (Gem) and 5-fluorouracil (5-FU), widely used anticancer drugs, lead to IL-1β secretion releasing cathepsin B which activates Nlrp3 inflammasome in myeloid derived suppressor cells (MDSCs). MDSC derived IL-1β enhance secretion of IL-17 by CD4+ T cells. This mechanism limits the antitumor efficacy of the drugs and promotes tumor growth.

Keywords: Gemcitabin, 5-fluorouracil, MDSCs, Nlrp3 inflammasome

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