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PD-L1 Enhanced by cis-Urocanic Acid on Langerhans Cells Inhibits Vg4+ gdT17 Cells in Psoriatic Skin Inflammation

ABSTRACT: PD-L1 Enhanced by cis-Urocanic Acid on Langerhans Cells Inhibits Vg4+ gdT17 Cells in Psoriatic Skin Inflammation

PROVIDER: PRJNA918579 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22984500.fastq.gz	Fastqsanger.gz
	SRR22984501.fastq.gz	Fastqsanger.gz
	SRR22984502.fastq.gz	Fastqsanger.gz
	SRR22984496.fastq.gz	Fastqsanger.gz
	SRR22984497.fastq.gz	Fastqsanger.gz

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PD-L1 Enhanced by cis-Urocanic Acid on Langerhans Cells Inhibits Vg4+ gdT17 Cells in Psoriatic Skin Inflammation

Project description:To establish the role of PD-L1 expression on Langerhans cells and its influence on psoriatic skin inflammation, we isolated Langerhans cells from harvested ears of wild type mice treated with Vaseline or Imiquimod. We then determined the gene expression profile of isolated Langerhans cells from the different groups at a single time point using data from RNA-seq. The experiment was performed in duplicate.

2023-06-30 | GSE222197 | GEO

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Project description:The aim of this experiment was to decipher the role of retinoic acid receptor (RAR) on interleukin(IL)-17-producing gamma delta (gdT17) T cells. Therefore we generated mice where RAR activity is defective specifically in cells expressing the transcription factor RORgt, which is constitutively on in gdT17 cells. From these mice and their littermate controls we FACS-sorted the two major gdT17 populations from the lymph node (Vg4+ and Vg4-) and subjected them to RNA-seq.

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RNA-sequencing of Vg4+Vd4+gdT cells isolated from skin-draining lymph nodes of WT and NF-kB1 deficient mice after imiquiod treatment

Project description:Purpose: The numbers of Vg4+Vd4+gdT17 cells in skin-draining lymph nodes were significantly reduced in imiqimod-treated NF-kB1-/- mice compared to those in IMQ-treated WT mice. To address the mechanism of NF-kB1-mediated proliferation of Vg4+Vd4+gdT17 cells, we performed RNA-sequencing of Vg4+Vd4+gdT cells isolated from the draining lymph nodes. Method: Mice were treated daily with 50 mg of 5% imiquimod cream or sham cream on both ears for 4 days. Single cell suspensions were separated from cervical lymph nodes. Vg4+Vd4+gdT cells were isolated by a cell sorter. N=3 each. Results: Using an optimized data analysis workflow, 552 of the transcripts showed differential expression between the WT and NF-kB1 deficient mice after imiquiod treatment, with a fold change ≥2 and p value <0.05.

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Serotonin 2A Receptor Attenuates Psoriatic Inflammation by Suppressing IL-23 Secretion in Monocyte-derived Langerhans cells

Project description:Serotonin and its receptor are known to play a role in regulating immune cells. However, how they affect an autoimmune disease like psoriasis is not well-established and the mechanism remains to be elucidated. Here, we investigated the role played by serotonin 2A receptor (HTR2A) in regulating psoriasis. HTR2A antagonistic drug worsens psoriatic outcome and HTR2A modulation reduced psoriatic inflammation. Using Imiquimod-induced psoriasiform inflammation model, HTR2A-deficient mice experienced exacerbated inflammation. Hematopoietic cells, particularly monocyte-derived Langerhans cells, were responsible for this exacerbated inflammation. Mechanistically, the exacerbated inflammation is due to increased interleukin-23 (IL-23) secretion and HTR2A suppresses it by inhibiting the activation of non-canonical NFkB pathway. Platelet-derived serotonin is the putative agonist modulating HTR2A attenuating psoriatic inflammation. Lastly, our findings in mice were also reproduced clinically. Thus, our data demonstrate platelet serotonin putatively modulates HTR2A attenuating psoriatic inflammation by suppressing IL-23 secretion via inhibiting non-canonical NFkB pathway in monocyte-derived Langerhans cells.

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Serotonin 2A Receptor Attenuates Psoriatic Inflammation by Suppressing IL-23 Secretion in Monocyte-derived Langerhans cells (mouse)

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Project description:Psoriasis is a chronic inflammatory skin disease of unknown etiology. Although macrophages and dendritic cells (DCs) have been proposed to drive the psoriatic cascade, their largely overlapping phenotype hampered studying their respective role. Topical application of Imiquimod, a Toll-like receptor 7 agonist, induces psoriasis in patients and psoriasiform inflammation in mice. We showed that daily application of Imiquimod for 14 days recapitulated both the initiation and the maintenance phase of psoriasis. Based on our ability to discriminate Langerhans cells (LCs), conventional DCs, monocytes, monocyte-derived DCs and macrophages in the skin, we characterized their dynamics during both phases of psoriasis. During the initiation phase, neutrophils infiltrated the epidermis whereas monocytes and monocyte-derived DCs were predominant in the dermis. During the maintenance phase, LCs and macrophage numbers increased in the epidermis and dermis, respectively. LC expansion resulted from local proliferation, a conclusion supported by transcriptional analysis. Continuous depletion of LCs during the course of Imiquimod treatment aggravated chronic psoriatic symptoms as documented by an increased influx of neutrophils and a stronger inflammation. Therefore, by developing a mouse model that mimics the human disease more accurately, we established that LCs play a negative regulatory role during the maintenance phase of psoriasis.

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Serotonin 2A Receptor Attenuates Psoriatic Inflammation by Suppressing IL-23 Secretion in Monocyte-derived Langerhans cells

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Project description:Serotonin 2A Receptor Attenuates Psoriatic Inflammation by Suppressing IL-23 Secretion in Monocyte-derived Langerhans cells (mouse)

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