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Mus musculus

ABSTRACT: RNA sequencing, Type XVII collagen-specific CD4+ T cells induce bullous pemphigoid by producing

PROVIDER: PRJDB16973 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR511613.fastq.gz	Fastqsanger.gz
	DRR511614.fastq.gz	Fastqsanger.gz
	DRR511615.fastq.gz	Fastqsanger.gz
	DRR511616.fastq.gz	Fastqsanger.gz
	DRR511617.fastq.gz	Fastqsanger.gz

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BP180 dysfunction triggers spontaneous skin inflammation in mice

Project description:BP180, also known as collagen XVII, is a hemidesmosomal component and plays a key role in 2 maintaining skin dermal/epidermal adhesion. Dysfunction of BP180, either through genetic 3 mutations in Junctional Epidermolysis Bullosa (JEB) or autoantibody insult in Bullous Pemphigoid 4 (BP), leads to subepidermal blistering accompanied by skin inflammation. However, whether BP180 5 is involved in skin inflammation remains unknown. To address this question, we generated a BP180-6 dysfunctional mouse strain and found that mice lacking functional BP180 (termed ΔNC16A) 7 developed spontaneous skin inflammatory disease, characterized by severe itch, defective skin 8 barrier, infiltrating immune cells, elevated serum IgE levels and increased expression of thymic 9 stromal lymphopoietin (TSLP). Severe itch is independent of adaptive immunity and histamine, but 10 dependent on increased expression of TSLP by keratinocytes. Our data provide the first direct 11 evidence showing that BP180 regulates skin inflammation independently of adaptive immunity, and 12 BP180 dysfunction leads to a TSLP mediated itch.

2018-03-23 | GSE112235 | GEO

Bulk RNA-seq of primary keratinocytes treated with IgG from patients with bullous pemphigoid or controls II

Project description:While antibodies in bullous pemphigoid (BP) are known to activate innate immune response, their direct effect on keratinocytes and the overall contribution of keratinocytes to disease pathogenesis is largely unknown. We sought to understand the mechanism of keratinocyte response to autoantibodies in BP. We affinity purified IgG from patients with a known diagnosis of bullous pemphigoid or healthy controls, and performed bulk RNA-seq. We identified numerous differentially expressed genes including upregulation of CXCL16, IL-24, and TGFB1 in BP-IgG treated keratinocytes

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Bulk RNA-seq of primary keratinocytes treated with IgG from patients with bullous pemphigoid or controls I

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Human gut

Project description:The gut microbiome in bullous pemphigoid

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Autoantigen-specific CD4+ T cells acquire an exhausted phenotype and persist in human antigen-specific autoimmune diseases

Project description:Pro-inflammatory autoantigen-specific CD4+ T helper (auto-Th) cells are central orchestrators of autoimmune diseases (AIDs). We aimed to characterize these cells in human AIDs with defined autoantigens by combining human leukocyte antigen (HLA)-tetramer-based and activation-based multidimensional ex vivo analyses. In aquaporin4-antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD) patients, auto-Th cells expressed CD154, but proliferative capacity and pro-inflammatory cytokines were strongly reduced. Instead, exhaustion-associated co-inhibitory receptors were expressed together with FOXP3, the canonical regulatory T cell (Treg) transcription factor. Auto-Th cells responded in vitro to checkpoint inhibition and provided potent B cell help. Cells with the same exhaustion-like (ThEx) phenotype were identified in soluble liver antigen (SLA)-antibody-autoimmune hepatitis and BP180-antibody-positive bullous pemphigoid, AIDs of the liver and skin, respectively. While originally described in cancer and chronic infection, our data point to T cell exhaustion as a common mechanism of adaptation to chronic (self-)stimulation across AID types and link exhausted CD4+ T cells to humoral autoimmune responses, with implications for therapeutic targeting.

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Skin metagenome

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Expression data in CD4 T cells from lungs of PBS or house dust mite treated mice

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Project description:Tertiary lymphoid tissues (TLTs) are formed in systemic organs manifesting chronic inflammation. Herein, we found that the renal pelvis (RP) could form urinary tract-associated lymphoid tissues (UTALTs) in a TLT-formation manner in humans and mice with chronic kidney disease (CKD), regardless of infectious pyelonephritis. Furthermore, collagen type XVII alpha 1 chain (COL17A1), localized ectopically to the transitional epithelium (TE) covering the UTALT, where it participated in TE development via immunological stimulation of UTALT-forming cells.

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Project description:We searched for candidate genes responsible for Epithelial-to-mesenchymal transition (EMT) by microarray analysis of cultured lung cancer cells with or without the property of spheroid formation. We found increased expression of a variety of adhesion molecules in cancer stem-like cells, including Collagen XVII. Further functional assays and signaling pathway were also investigated.

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