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Treatment and molecular analysis of bullous pemphigoid with tofacitinib: a case report and review of current literature

ABSTRACT: Treatment and molecular analysis of bullous pemphigoid with tofacitinib: a case report and review of current literature

PROVIDER: PRJNA1169756 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30918761_1.fastq.gz	Fastqsanger.gz
	SRR30918761_2.fastq.gz	Fastqsanger.gz
	SRR30918762_1.fastq.gz	Fastqsanger.gz
	SRR30918762_2.fastq.gz	Fastqsanger.gz
	SRR30918763_1.fastq.gz	Fastqsanger.gz

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Treatment and molecular analysis of bullous pemphigoid with tofacitinib: a case report and review of current literature

Project description:Bullous pemphigoid (BP) is a rare, life-threatening autoimmune blistering disease with pruritus and tension blisters/bullous as the main clinical manifestations. Glucocorticosteroids are the main therapeutic agents for it, but their efficacy is poor in some patients. Tofacitinib, a small molecule agent that inhibits JAK1/3, has shown incredible efficacy in a wide range of autoimmune diseases and maybe a new valuable treatment option for refractory BP. To report a case of refractory BP successfully treated with tofacitinib, then explore the underlying mechanism behind the treatment, and finally review similarities to other cases reported in the literature. Case report and literature review of published cases of successful BP treatment with JAK inhibitors. The case report describes a 73-year-old male with refractory BP that was successfully managed with the combination therapy of tofacitinib and low-dose glucocorticoids for 28 weeks. Immunohistochemistry and RNA sequencing were performed to analyze the underlying mechanism of tofacitinib therapy. A systematic literature search was conducted to identify other cases of treatment with JAK inhibitors. Throughout the 28-week treatment period, the patient experienced clinical, autoantibody and histologic resolution. Immunohistochemical analysis showed tofacitinib significantly decreased the pSTAT3 and pSTAT6 levels in the skin lesions of this patient. RNA sequencing and immunohistochemical testing of lesion samples from other BP patients identified activation of the JAK-STAT signaling pathway. Literature review revealed 17 previously reported cases of BP treated with four kinds of JAK inhibitors successfully, including tofacitinib (10), baricitinib (1), upadacitinib (3) and abrocitinib (3). Our findings support the potential of tofacitinib as a safe and effective treatment option for BP. Larger studies are underway to better understand this efficacy and safety.

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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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Project description:Large-scale transcriptome and methylome data analyses obtained by high-throughput technologies have been enabling the identification of novel imprinted genes. We investigated genome-wide DNA methylation patterns in multiple human tissues, using a high-resolution microarray to uncover hemimethylated CpGs located in promoters overlapping CpG islands, aiming to identify novel candidate imprinted genes. Using our approach, we recovered ~30% of the known human imprinted genes, further 168 candidates were identified, 61 of which with at least three hemimethylated CpGs shared by more than two tissue types. Thirty-four of these candidate genes are members of the protocadherins cluster on 5q31.3; in mice, protocadherin genes have non-imprinted monoallelic randomic expression, which might be the case in humans. Among the remaining 27 genes, ZNF331 was recently validated as an imprinted gene, and six of them have been reported as candidates, supporting our prediction. Five candidates (CCDC166, ARC, PLEC, TONSL and VPS28) map to 8q24.3, and might constitute a novel imprinted cluster. Additionally, we performed a comprehensive compilation of known human and mice imprinted genes from literature and databases, and a comparison among high-throughput imprinting studies in humans. The screening for hemimethylated CpGs shared by multiple human tissues, together with the extensive review, appears as a useful approach to reveal candidate imprinted genes.

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