scholarly journals Regulatory Innate Lymphoid Cells: A new subset of innate immune lymphocytes with more potential functions to be discovered in immune regulation

Author(s):  
Jifeng Yu

Regulatory innate lymphoid cells (ILCregs) are a newly identified subset of innate immune lymphocytes. The discovery of this subset cell has revealed several inhibitory and stimulatory pathways that affect the regulatory functions of ILCregs, in addition to miRNA and other genetic molecular regulations. These pathways may play important roles in the pathogenesis and potential immunotherapy in patients with different kind of diseases, such as inflammation and ischemia / reperfusion injury of the kidney, acute myeloid leukemia, through immunomodulatory and anti-inflammatory pathway, as well as miRNA regulations. Further studies on ILCregs may be a potentially high interest in the near future.

2021 ◽  
Vol 12 ◽  
Author(s):  
Wenling Yang ◽  
Jibin Lin ◽  
Jin Zhou ◽  
Yuqi Zheng ◽  
Shijiu Jiang ◽  
...  

Myocardial infarction results from obstruction of a coronary artery that causes insufficient blood supply to the myocardium and leads to ischemic necrosis. It is one of the most common diseases threatening human health and is characterized by high morbidity and mortality. Atherosclerosis is the pathological basis of myocardial infarction, and its pathogenesis has not been fully elucidated. Innate lymphoid cells (ILCs) are an important part of the human immune system and participate in many processes, including inflammation, metabolism and tissue remodeling, and play an important role in atherosclerosis. However, their specific roles in myocardial infarction are unclear. This review describes the current understanding of the relationship between innate lymphoid cells and myocardial infarction during the acute phase of myocardial infarction, myocardial ischemia-reperfusion injury, and heart repair and regeneration following myocardial infarction. We suggest that this review may provide new potential intervention targets and ideas for treatment and prevention of myocardial infarction.


2019 ◽  
Vol 10 ◽  
Author(s):  
Guy J. M. Cameron ◽  
Kelly M. Cautivo ◽  
Svenja Loering ◽  
Simon H. Jiang ◽  
Aniruddh V. Deshpande ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Babak Baban ◽  
Hesam Khodadadi ◽  
Kumar Vaibhav ◽  
Cristina Marchetti ◽  
Carlo Riccardi ◽  
...  

Innate lymphoid cells (ILCs) have emerged as largely tissue-resident archetypal cells of the immune system. We tested the hypotheses that renal ischemia-reperfusion injury (IRI) is a contributing factor to polarization of ILCs and that glucocorticoid-induced leucine zipper (GILZ) and cannabidiol regulate them in this condition. Mice subjected to unilateral renal IRI were treated with the following agents before restoration of renal blood flow: cannabidiol, DMSO, transactivator of transcription- (TAT-) GILZ, or the TAT peptide. Thereafter, kidney cells were prepared for flow cytometry analyses. Sham kidneys treated with either cannabidiol or TAT-GILZ displayed similar frequencies of each subset of ILCs compared to DMSO or TAT, respectively. Renal IRI increased ILC1s and ILC3s but reduced ILC2s compared to the sham group. Cannabidiol or TAT-GILZ treatment of IRI kidneys reversed this pattern as evidenced by reduced ILC1s and ILC3s but increased ILC2s compared to their DMSO- or TAT-treated counterparts. While TAT-GILZ treatment did not significantly affect cells positive for cannabinoid receptors subtype 2 (CB2+), cannabidiol treatment increased frequency of both CB2+ and GILZ-positive (GILZ+) cells of IRI kidneys. Subsequent studies showed that IRI reduced GILZ+ subsets of ILCs, an effect less marked for ILC2s. Treatment with cannabidiol increased frequencies of each subset of GILZ+ ILCs, but the effect was more marked for ILC2s. Indeed, cannabidiol treatment increased CB2+ GILZ+ ILC2s. Collectively, the results indicate that both cannabidiol and GILZ regulate ILC frequency and phenotype, in acute kidney injury, and that the effects of cannabidiol likely relate to modulation of endogenous GILZ.


2017 ◽  
Vol 199 (8) ◽  
pp. 2921-2929 ◽  
Author(s):  
Mayya Geha ◽  
Maria G. Tsokos ◽  
Robin E. Bosse ◽  
Tatyana Sannikova ◽  
Yoichiro Iwakura ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Dongwei Xu ◽  
Yizhu Tian ◽  
Qiang Xia ◽  
Bibo Ke

Liver diseases represent a major global health burden accounting for approximately 2 million deaths per year worldwide. The liver functions as a primary immune organ that is largely enriched with various innate immune cells, including macrophages, dendritic cells, neutrophils, NK cells, and NKT cells. Activation of these cells orchestrates the innate immune response and initiates liver inflammation in response to the danger signal from pathogens or injured cells and tissues. The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is a crucial signaling cascade of the innate immune system activated by cytosol DNA. Recognizing DNA as an immune-stimulatory molecule is an evolutionarily preserved mechanism in initiating rapid innate immune responses against microbial pathogens. The cGAS is a cytosolic DNA sensor eliciting robust immunity via the production of cyclic GMP-AMPs that bind and activate STING. Although the cGAS-STING pathway has been previously considered to have essential roles in innate immunity and host defense, recent advances have extended the role of the cGAS-STING pathway to liver diseases. Emerging evidence indicates that overactivation of cGAS-STING may contribute to the development of liver disorders, implying that the cGAS-STING pathway is a promising therapeutic target. Here, we review and discuss the role of the cGAS-STING DNA-sensing signaling pathway in a variety of liver diseases, including viral hepatitis, nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), primary hepatocellular cancer (HCC), and hepatic ischemia-reperfusion injury (IRI), with highlights on currently available therapeutic options.


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