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IL-8 drives the differentiation of CD74high neutrophils to activate anti-tumor immunity and attenuate NSCLC progression

ABSTRACT: IL-8 drives the differentiation of CD74high neutrophils to activate anti-tumor immunity and attenuate NSCLC progression

PROVIDER: PRJNA1060686 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27238768_1.fastq.gz	Fastqsanger.gz
	SRR27238768_2.fastq.gz	Fastqsanger.gz
	SRR27238769_1.fastq.gz	Fastqsanger.gz
	SRR27238769_2.fastq.gz	Fastqsanger.gz
	SRR27238770_1.fastq.gz	Fastqsanger.gz

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IL-8 drives the differentiation of CD74high neutrophils to activate anti-tumor immunity and attenuate NSCLC progression [II]

Project description:Neutrophils infiltrated in the tumor microenvironment (TME) are heterogeneous populations associated with the prognosis of cancer and cancer immunotherapy. However, the plasticity and function of heterogeneous neutrophils in the TME of non-small cell lung cancer (NSCLC) remain poorly understood. Here, we show that neutrophils produce high levels of IL-8 which induce the differentiation of CD74highSiglecFlow neutrophils and suppress the generation of CD74lowSiglecFhigh neutrophils in the TME of IL-8-humanized (IL8-hu) KrasLSL-G12DTp53fl/fl (KP) and EGFRT790M/Del-Exon19 (EGFRTD) NSCLC mouse models. The CD74highSiglecFlow neutrophils exhibit antigen cross-presentation activity to augment anti-tumor T cell responses. Consistently, deletion of CD74 in IL8-hu neutrophils attenuates the activation of T cells and exacerbates the progression of NSCLC, whereas treatment of a CD74 agonist promotes anti-tumor T cell activation and enhances the effects of anti-PD1 or Osimertinib therapy in the IL8-hu NSCLC mouse models. In addition, we have found that the CD74highCD63low neutrophils in the TME and peripheral blood of advanced NSCLC patients pheno-copy the CD74highSiglecFlow neutrophils in the TME of NSCLC mice and correlate well with the responsiveness to anti-PD-1 plus chemotherapies. Collectively, these data demonstrate an IL-8-CD74high neutrophil axis that promotes anti-tumor immunity in NSCLC.

2024-09-13 | GSE252460 | GEO

IL-8 drives the differentiation of CD74high neutrophils to activate anti-tumor immunity and attenuate NSCLC progression [I]

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IL-8 drives the differentiation of CD74high neutrophils to activate anti-tumor immunity and attenuate NSCLC progression [I]

Project description:IL-8 drives the differentiation of CD74high neutrophils to activate anti-tumor immunity and attenuate NSCLC progression [I]

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IL-8 drives the differentiation of CD74high neutrophils to activate anti-tumor immunity and attenuate NSCLC progression [II]

Project description:IL-8 drives the differentiation of CD74high neutrophils to activate anti-tumor immunity and attenuate NSCLC progression [II]

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IL-8 drives the differentiation of CD74high neutrophils to activate anti-tumor immunity and attenuate NSCLC progression

Project description:This SuperSeries is composed of the SubSeries listed below.

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SARS-CoV-2-associated ssRNAs activate human neutrophils in a TLR8-dependent fashion

Project description:COVID-19 disease is characterized by a dysregulation of the innate arm of the immune system. However, the mechanisms whereby innate immune cells, including neutrophils, become activated in patients are not completely understood. Recently, we showed that a GU-rich RNA sequence from SARS-CoV-2 genome (i.e., SCV2-RNA2) activates dendritic cells. To clarify whether human neutrophils may also represent targets of SCV2-RNA2, neutrophils were treated with either SCV2-RNA2 or, as control, R848 (a TLR7/8 ligand), and then analysed for several functional assays and also subjected to RNA-seq experiments. Results highlight a remarkable response of neutrophils to SCV2-RNA2 in terms of TNFa, IL1ra, CXCL8 production, apoptosis delay, modulation of CD11b and CD62L expression and release of neutrophil extracellular traps. By RNA-seq experiments, we observed that SCV2-RNA2 promotes a transcriptional reprogramming of neutrophils, characterized by the induction of thousands of proinflammatory genes, similarly to that promoted by R848. Furthermore, by using CU-CPT9a, a TLR8-specific inhibitor, we found that SCV2-RNA2 stimulates neutrophils exclusively via TLR8-dependent pathways. In sum, our study proves that single-strand RNAs from the SARS-CoV-2 genome potently activate human neutrophils via TLR8, thus uncovering a potential mechanism whereby neutrophils may contribute to the pathogenesis of severe COVID-19 disease.

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