Resistance to Chemotherapy on Tumor Through Cathepsin B-dependent Activation of the NLRP3 Inflammasome.
10.4167/jbv.2013.43.3.233
- Author:
Eun Jeong KWON
1
;
Young Sang KOH
Author Information
1. Jeju National University School of Medicine, Jeju, Korea. yskoh7@jejunu.ac.kr
- Publication Type:Letter
- Keywords:
Gemcitabin;
5-fluorouracil;
MDSCs;
Nlrp3 inflammasome
- MeSH:
Cathepsin B;
Cathepsins;
Fluorouracil;
Interleukin-17;
T-Lymphocytes
- From:Journal of Bacteriology and Virology
2013;43(3):233-234
- CountryRepublic of Korea
- Language:Korean
-
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-1beta secretion releasing cathepsin B which activates Nlrp3 inflammasome in myeloid derived suppressor cells (MDSCs). MDSC derived IL-1beta enhance secretion of IL-17 by CD4+ T cells. This mechanism limits the antitumor efficacy of the drugs and promotes tumor growth.
