- 作者: Vijay Kumar, Caitlin Bauer & John H. Stewart IV
- 作者服務機構: 1.Department of Interdisciplinary Oncology, Stanley S. Scott Cancer Center, School of Medicine, Louisiana State University Health Science Center (LSUHSC), 1700 Tulane Avenue, New Orleans, LA, 70012, USA 2.Louisiana Children’s Medical Center Cancer Center, Stanley S. Scott Cancer Center, School of Medicine, Louisiana State University Health Science Center (LSUHSC), 1700 Tulane Avenue, New Orleans, LA, 70012, USA 3.Surgery, Section of Surgical Oncology, Louisiana State University New Orleans-Louisiana Children’s Medical Center Cancer Center, Louisiana State University Health Science Center (LSUHSC), 1700 Tulane Avenue, New Orleans, LA, 70012, USA
- 中文摘要:
- 英文摘要:
Myeloid immune cells (MICs) are potent innate immune cells serving as frst responders to invading pathogens
and internal changes to cellular homeostasis. Cancer is a stage of altered cellular homeostasis that can originate
in response to diferent pathogens, chemical carcinogens, and internal genetic/epigenetic changes. MICs express
several pattern recognition receptors (PRRs) on their membranes, cytosol, and organelles, recognizing systemic, tissue, and organ-specifc altered homeostasis. cGAS/STING signaling is a cytosolic PRR system for identifying cytosolic
double-stranded DNA (dsDNA) in a sequence-independent but size-dependent manner. The longer the cytosolic
dsDNA size, the stronger the cGAS/STING signaling activation with increased type 1 interferon (IFN) and NF-κBdependent cytokines and chemokines’ generation. The present article discusses tumor-supportive changes occurring
in the tumor microenvironment (TME) or tumor immune microenvironment (TIME) MICs, specifcally emphasizing
cGAS/STING signaling-dependent alteration. The article further discusses utilizing MIC-specifc cGAS/STING signaling
modulation as critical tumor immunotherapy to alter TIME. - 中文關鍵字:
- 英文關鍵字: s Cancer, cGAS, STING, MIC, Macrophages, DCs, MDSCs, TME, TIME