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Mechanisms regulating transitory suppressive activity of neutrophils in newborns

ABSTRACT: Mechanisms regulating transitory suppressive activity of neutrophils in newborns

PROVIDER: PRJNA835206 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19090401.fastq.gz	Fastqsanger.gz
	SRR19090402.fastq.gz	Fastqsanger.gz
	SRR19090403.fastq.gz	Fastqsanger.gz
	SRR19090404.fastq.gz	Fastqsanger.gz
	SRR19090405.fastq.gz	Fastqsanger.gz

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Mechanisms regulating transitory suppressive activity of neutrophils in newborns

Project description:Transitory appearance of immune suppressive polymorphonuclear neutrophils (PMN) defined as myeloid-derived suppressor cells (PMN-MDSC) in newborns is important for their protection from inflammation associated with newly established gut microbiota. Here, we report that inhibition of the type I interferon (IFN1) pathway played a major role in regulation of PMN-MDSC suppressive activity during first weeks of life. Expression of the IFN1 receptor IFNAR1 was markedly lower in PMN-MDSC. However, in newborn mice, down-regulation of IFNAR1 was not sufficient to render PMN immune suppressive. That also required the presence of a positive signal from lactoferrin via its receptor LRP2. The latter effect was mediated via NF-kB activation, which was tempered by IFN1 in a manner that involved SOCS3. Thus, we discovered a mechanism of tight regulation of immune suppressive PMN-MDSC in newborns, which may be used in the development of therapies of neonatal pathologies

2022-05-31 | GSE202264 | GEO

Mechanisms regulating transitory suppressive activity of neutrophils in newborns: PMNs-MDSCs in newborns.

Project description:Transitory appearance of immune suppressive polymorphonuclear neutrophils (PMNs) defined as myeloid-derived suppressor cells (PMNs-MDSCs) in newborns is important for their protection from inflammation associated with newly established gut microbiota. Here, we report that inhibition of the type I IFN (IFN1) pathway played a major role in regulation of PMNs-MDSCs-suppressive activity during first weeks of life. Expression of the IFN1 receptor IFNAR1 was markedly lower in PMNs-MDSCs. However, in newborn mice, down-regulation of IFNAR1 was not sufficient to render PMNs immune suppressive. That also required the presence of a positive signal from lactoferrin via its receptor low-density lipoprotein receptor-related protein 2. The latter effect was mediated via NF-κB activation, which was tempered by IFN1 in a manner that involved suppressor of cytokine signaling 3. Thus, we discovered a mechanism of tight regulation of immune suppressive PMNs-MDSCs in newborns, which may be used in the development of therapies of neonatal pathologies.

| S-EPMC9794389 | biostudies-literature

Fatty acid transporter 2 regulates lipid metabolism and suppressive function of neutrophils in cancer

Project description:Polymorphonuclear myeloid derived suppressor cells (PMN-MDSC) are pathologically activated neutrophils that accumulate in cancer and many other pathologic conditions. PMN-MDSC are critically important for the regulation of immune responses in cancer, promotion of tumor progression, and metastases. Despite the recent advances in understanding of the PMN-MDSC biology, the mechanisms responsible for pathological activation of neutrophils are not well defined, which limit selective targeting of PMN-MDSC. Here, we report that mouse and human PMN-MDSC exclusively up-regulate fatty acid transporter protein 2 (FATP2). Over-expression of FATP2 in PMN-MDSC was controlled by GM-CSF, through the activation of STAT5 transcription factor. Genetic ablation of FATP2 abrogated the suppressive activity of PMN-MDSC in spleens and tumors. FATP2 in neutrophils promoted accumulation of oxidized lipids. However, the main mechanism of FATP2 mediated suppressive activity of PMN-MDSC involved uptake of arachidonic acid and synthesis of prostaglandin E2. The selective pharmacological inhibition of FATP2 abrogated activity of PMN-MSC and substantially delayed tumor progression. In combination with check-point inhibitors it blocked tumor progression in mice. Thus, FATP2 mediates acquisition of immune suppressive activity by PMN-MDSC and represents a new target to inhibit the functions of PMN-MDSC and improve the effect of immunotherapy of cancer.

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Immune suppressive activity of myeloid-derived suppressor cells in cancer requires inactivation of the type I interferon pathway

Project description:Myeloid-derived suppressor cells (MDSC) are pathologically activated neutrophils and monocytes with potent immune suppressive activity. These cells play an important role in accelerating tumor progression and undermining the efficacy of anti-cancer therapies. The natural mechanisms limiting MDSC activity are not well understood. Here, we present evidence that type I interferons (IFN1) receptor signaling serves as a universal mechanism that restricts acquisition of suppressive activity by these cells. Downregulation of the IFNAR1 chain of this receptor was found in MDSC from cancer patients and mouse tumor models. The decrease in IFNAR1 depended on the activation of the p38 protein kinase and was required for activation of the immune suppressive phenotype. Whereas deletion of IFNAR1 was not sufficient to convert neutrophils and monocytes to MDSC, genetic stabilization of IFNAR1 in tumor bearing mice undermined suppressive activity of MDSC and had potent antitumor effect. Stabilizing IFNAR1 using inhibitor of p38 combined with the interferon induction therapy elicited a robust anti-tumor effect. Thus, negative regulatory mechanisms of MDSC function can be exploited therapeutically.

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Project description:Myeloid derived suppressor cells (MDSC) playing the immune suppressive roles in tumor bearing host consists of two major subsets of granulocytic and monocytic cells. Granulocytic MDSC (G-MDSC) express CD11b+ Gr-1high Ly6G+ Ly6Clow and produce high level of reactive oxygen species (ROS). Interestingly, neutrophils are well known ROS producing cells during immune defensive process and share same surface markers with G-MDSC. These similar features always brought the fundamental questions what’s the difference between G-MDSC and neutrophils but it’s not yet proven clearly. In this study, we examined the gene expression of G-MDSC and neutrophils using Affymetrix microarray G-MDSC (CD11b+Ly6G+Ly6Clow) were purifed from splenocytes in EL4 lymphoma tumor bearing mice by positive selection of Ly6G using microbeads isolation. Neutrophils were purified from ascitic fluids induced after injection of milk protein, casein by negative selection of F4/80 and positive selection of Ly6G using microbeads isolation. Their RNA was extracted and gene expression was analyzed using Affymetrix microarray.

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