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Effect of laminin-332 pemphigoid IgG on the keratinocyte transcriptome

ABSTRACT: To determine the role of laminin-332 autoantibodies in inducing a pro-inflammatory and proteolytic response by keratinocytes

ORGANISM(S): Homo sapiens

PROVIDER: GSE182644 | GEO | 2021/08/26

REPOSITORIES: GEO

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Effect of laminin-332 pemphigoid IgG on the keratinocyte transcriptome

Project description:Effect of laminin-332 pemphigoid IgG on the keratinocyte transcriptome

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Intravenous immunoglobulin (IVIg) ameliorates disease in a murine model of anti-laminin 332 mucous membrane pemphigoid

Project description:Intravenous immunoglobulin (IVIg) is used to treat mucous membrane pemphigoid (MMP), although its therapeutic effectivity is not sufficiently supported by randomized controlled clinical trials and its mode of action is only insufficiently understood. We have examined the effect of IVIg in a mouse model of anti-laminin 332 MMP and found that IVIg ameliorates both cutaneous and mucosal inflammatory lesions. Our investigation into the modes of action of IVIg in MMP indicated effective antiinflammatory mechanisms beyond the enhanced degradation of IgG mediated through inhibition of the neonatal Fc receptor. Our results suggest that IVIg curbs the activation of neutrophils at several levels. This includes a direct, immediate inhibitory effect on neutrophil activation by immune complexes but not C5a which blunts the release of reactive oxygen species and leukotriene B4 from neutrophils. IVIg also suppresses the formation of neutrophil extracellular traps in response to Ca2+ ionophore. In vivo treatment with IVIg altered the transcriptome of blood leukocytes and bone marrow neutrophils towards less proinflammatory phenotypes. Collectively, our results support the effectivity of IVIg in the treatment of MMP and indicate that effects on neutrophils at multiple levels may significantly contribute to its therapeutic effects.

2024-04-10 | GSE263026 | GEO

Effect of full-length laminin 332 treatment on the transcriptome of mouse keratinocytes that express or lack integrin α3β1

Project description:Basement membrane protein Laminin-332 (LN332) is upregulated after injury and promotes keratinocyte migration. It functions as a key ligand for integrin α3β1, which is highly expressed by basal keratinocytes and further induced after wounding. Integrin α3β1 has been previously demonstrated to be a major regulator of the keratinocyte transcriptome. Here, we investigated whether topical application of recombinant full-length LN332 wound impact the keratinocyte transcriptome, and whether integrin α3β1 expression would be required for LN332's effect. It is important to note that keratinocytes make and secrete LN332, therefore the genes that respond to LN332 treatment are responding to treatment with additional (exogenous) recombinant LN332 and likely represent a small fraction of the genes that are regulated by the endogenous LN332-α3β1 axis.

2026-06-29 | GSE336489 | GEO

Intravenous immunoglobulin (IVIg) ameliorates disease in a murine model of anti-laminin 332 mucous membrane pemphigoid

Project description:Intravenous immunoglobulin (IVIg) ameliorates disease in a murine model of anti-laminin 332 mucous membrane pemphigoid

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RNA sequencing from epidermis of LAMA3-deficient mice

Project description:RNA sequencing data of mouse epidermis isolated from wild type and LAMA3-deficient mice Genetic, clinical and biochemical studies concurred to establish that integrity of the dermal-epidermal junction requires laminin 332, a particular subset of epithelial laminins. Laminin 332 is composed of three subunits, α3, β3 and γ2, encoded by the Lama3, Lamb3 and Lamc2 genes, respectively. In vivo functional analysis of laminin 332 in skin has been prevented because constitutive mutations of any one of the coding genes, either inherited in human or engineered in mice, cause junctional epidermolysis bullosa and early death. Consequently, it is still unknown whether and how laminin 332 contributes to skin homeostasis. To circumvent the problem, we have generated a mouse model in which disruption of the Lama3 gene is conditional and specifically induced in epidermal keratinocytes after birth. It causes a progressive depletion of laminin 332 in the skin of the mouse, which is compatible with life. To assess how laminin 332 supervises epidermal homeostasis, RNA was prepared from keratinocytes isolated from laminin 332-depleted skin and control animals (three each) to compare their gene expression profiles using RNA sequencing.

2021-02-18 | GSE146045 | GEO

Keratinocyte footprint assay discriminates antilaminin-332 pemphigoid from all other forms of pemphigoid diseases.

Project description: Not available

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

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

2024-12-04 | GSE280619 | GEO

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

2024-12-04 | GSE280620 | GEO

Comparison of Two Diagnostic Assays for Anti-Laminin 332 Mucous Membrane Pemphigoid.

Project description: Not available

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Effect of full-length laminin 332 treatment on the transcriptome of mouse keratinocytes that express or lack integrin α3β1

Project description:Effect of full-length laminin 332 treatment on the transcriptome of mouse keratinocytes that express or lack integrin α3β1

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