Targeting cGAS/STING signaling-mediated myeloid immune cell dysfunction in TIME

Journal of Biomedical Science

Review

Vijay Kumar¹  Caitlin Bauer¹  John H. Stewart² 

[1] Department of Interdisciplinary Oncology, Stanley S. Scott Cancer Center, School of Medicine, Louisiana State University Health Science Center (LSUHSC), 1700 Tulane Avenue, 70012, New Orleans, LA, USA;Department of Interdisciplinary Oncology, Stanley S. Scott Cancer Center, School of Medicine, Louisiana State University Health Science Center (LSUHSC), 1700 Tulane Avenue, 70012, New Orleans, LA, USA;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, 70012, New Orleans, LA, USA;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, 70012, New Orleans, LA, USA;

关键词: Cancer;    cGAS;    STING;    MIC;    Macrophages;    DCs;    MDSCs;    TME;    TIME;   

DOI  :  10.1186/s12929-023-00942-2

 received in 2023-04-03, accepted in 2023-06-14,  发布年份 2023

来源: Springer

【 摘 要 】

Myeloid immune cells (MICs) are potent innate immune cells serving as first responders to invading pathogens and internal changes to cellular homeostasis. Cancer is a stage of altered cellular homeostasis that can originate in response to different 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-specific 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-κB-dependent cytokines and chemokines’ generation. The present article discusses tumor-supportive changes occurring in the tumor microenvironment (TME) or tumor immune microenvironment (TIME) MICs, specifically emphasizing cGAS/STING signaling-dependent alteration. The article further discusses utilizing MIC-specific cGAS/STING signaling modulation as critical tumor immunotherapy to alter TIME.

【 授权许可】

CC BY   
© The Author(s) 2023

【 图 表 】

Fig. 6

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