作者: Fatma Saaoud , Daohai Yu , Rongshan Li , Shuping Ge , Candice Johnson
DOI: 10.1155/2021/6664453
关键词: Lius 、 Immune checkpoint 、 Proinflammatory cytokine 、 Innate immune system 、 Immune system 、 Inflammation 、 Heat generation 、 Biology 、 Cell biology 、 Acquired immune system
摘要: Background The immune mechanisms underlying low-intensity ultrasound- (LIUS-) mediated suppression of inflammation and tumorigenesis remain poorly determined. Methods We used microarray datasets from the NCBI GEO DataSet repository conducted comprehensive data-mining analyses, where we examined gene expression 1376 innate regulators (innatome genes (IGs) in cells treated with LIUS. Results made following findings: (1) LIUS upregulates proinflammatory IGs downregulates metastasis cancer cells, adaptive immunity pathways but inhibits danger-sensing promote tolerogenic differentiation bone marrow (BM) cells. (2) encoded for proteins localized cytoplasm, extracellular space, others, IG nuclear plasma membranes, phosphatases. (3) LIUS-modulated act partially via several important reactive oxygen species (ROS), reverse signaling checkpoint receptors B7-H4 BTNL2, inflammatory cytokines, static or oscillatory shear stress heat generation, among which ROS is a dominant mechanism. (4) trained enzymes lymphoma presumably establishes tolerance BM (5) modulates chromatin long-range interactions to differentially regulate noncancer Conclusions Our analysis suggests novel molecular that are utilized by induce tumor inhibition. findings may lead development new treatment protocols cancers chronic inflammation.