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In vitro stimulation of mouse spleen cells by COL17A1

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE151929 | GEO | 2022/01/26

REPOSITORIES: GEO

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Compared gene expression between kidney and renal pelvis

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. Our results demonstrated that urine is crucial for UTALT development. Urine leak from the lumen into the parenchyma of the RP through an altered transitional epithelium (TE) barrier, stimulated RP stromal cells immunologically and attracted immune cells via cytokine and chemokine production. Pathophysiological crosstalk was observed between UTALT development and tubulointerstitial lesions and TLT formation in the kidney.

2022-01-26 | GSE151930 | GEO

Hair follicle aging is driven by transepidermal stem cell elimination via COL17A1 proteolysis

Project description:Hair loss is one of the typical aging phenotypes in mammals, yet the underlying mechanism(s) is unclear. Here we report that hair follicle stem cell (HFSC) aging causes the stepwise miniaturization of hair follicles and eventual hair loss both in wild-type mice and in humans. In vivo fate analysis of HFSCs revealed that the DNA damage response in HFSCs causes proteolysis of Type XVII Collagen (COL17A1/BP180) to trigger “HFSC aging”, characterized by their loss of stemness signature and epidermal commitment. Those aged HFSCs are cyclically eliminated from the skin through their terminal epidermal differentiation, thereby causing hair follicle miniaturization. That process can be recapitulated by Col17a1 deficiency and prevented by forced maintenance of COL17A1 in HFSCs, demonstrating that stem cell homeostasis is the keystone against ultimate execution of the tissue/organ aging program.

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In vitro stimulation of mouse spleen cells by mouse urine

Project description:Urinary tract-associated lymphoid structures (UTLASs), tertiary lymphoid tissues, are formed in renal pelvis (RP) of humans and mice with chronic kidney disease. We found that UTALS development was accelerated by urine leakage from RP lumen to the parenchyma following dysfunction of transitional epithelium covering UTLASs. Thus, UTALS-forming cells were stimulated by urine including urinary bio active substances.

2024-04-15 | GSE207999 | GEO

The ureters of Col17a1-KO mice at 4 days after unilateral ureteral obsruction

Project description:Collagen 17A1 (COL17A1) is induced in urothelium under disease conditions of urinary system organs, such as chronic nephritis and urinary obstruction. Thus, the ureters of Col17a1-knock out (KO) mice were injured by unilateral ureteral obsruction (UUO), and the gene expression was compared with those of wild-tyoe (WT).

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Stem cell competition orchestrates skin homeostasis and ageing

Project description:Stem cells underlie tissue homeostasis, but their dynamics during ageing—and the relevance of these dynamics to organ ageing—remain unknown. Here we report that the expression of the hemidesmosome component collagen XVII (COL17A1) by epidermal stem cells fluctuates physiologically through genomic/oxidative stress-induced proteolysis, and that the resulting differential expression of COL17A1 in individual stem cells generates a driving force for cell competition. In vivo clonal analysis in mice and in vitro 3D modelling show that clones that express high levels of COL17A1, which divide symmetrically, outcompete and eliminate adjacent stressed clones that express low levels of COL17A1, which divide asymmetrically. Stem cells with higher potential or quality are thus selected for homeostasis, but their eventual loss of COL17A1 limits their competition, thereby causing ageing. The resultant hemidesmosome fragility and stem cell delamination deplete adjacent melanocytes and fibroblasts to promote skin ageing. Conversely, the forced maintenance of COL17A1 rescues skin organ ageing, thereby indicating potential angles for anti-ageing therapeutic intervention.

2019-04-05 | GSE111825 | GEO

In vitro stimulation of mouse spleen cells by COL17A1

Project description:In vitro stimulation of mouse spleen cells by COL17A1

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Immune Checkpoint Associated Acute Interstitial Nephritis

Project description:Tertiary lymphoid structure signatures are associated with immune checkpoint inhibitor related acute interstitial nephritis

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Lymphoid function of the tuberculous granuloma

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Infiltrating B cells and tertiary lymphoid structures in the TME

Project description:Single-cell profiling of infiltrating B cells and tertiary lymphoid structures in the TME of gastric adenocarcinomas

2021-11-22 | GSE188895 | GEO

Lymphoid Follicle Spatial Transcriptomics Resolve an Emphysema-Specific B Cell Signature in COPD

Project description:Using Geomx's Digital Space Profiling method for WTA RNA transcriptomics in lung tertiary lymphoid structures (TLS, follicles), we assessed paraffin-embedded and OCT-embedded lung sections from 48 patients, which were classified as Never Smoker Controls (NSC, n=8), Smoker Controls (SC, n=13), and COPD GOLD1-4 patients (n=27 patients). we identified 19 patients with tertiary lymphoid structures (TLS), distributed as 13 COPD patients and 6 SC subjects, with 115 TLS data used for the final data analysis.

2023-11-21 | GSE237120 | GEO

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