IL27 as a Novel Biomarker for Pruritus Specific in Nodular Prurigo and Bullous Pemphigoid
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ABSTRACT:
PROVIDER: PRJNA1166908 | ENA |
REPOSITORIES: ENA
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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:Background: Chronic nodular prurigo (CNPG) is a chronic inflammatory skin disease that is maintained by a chronic itch-scratch cycle likely rooted in neuro-immunological dysregulation. This condition may be associated with atopy in some patients, and there are now promising therapeutic results from blocking type-2 cytokines such as IL-4, IL-13 and IL-31. Nevertheless, underlying pathomechanisms as well as the molecular relationship with atopy remain ill-defined. Methods: We profiled skin lesions from patients with CNPG in comparison to atopic dermatitis (AD) and healthy control (HC) individuals using single-cell RNA sequencing combined with T-cell receptor sequencing. Results: We found type-2 immune skewing in both CNPG and AD, as evidenced by CD4+ helper T cells expressing IL13. However, only AD harbored an additional, oligoclonally expanded CD8A+ IL9R+ IL13+ cytotoxic T cell population, and immune activation pathways were highly upregulated in AD, but less so in CNPG. Conversely, CNPG showed signatures of extracellular matrix organization, collagen synthesis, and fibrosis, including a unique population of CXCL14- IL24+ secretory-papillary fibroblasts. Besides known itch mediators such as IL31 and oncostatin M (OSM), we also detected increased levels of neuromedin B (NMB) in fibroblasts of CNPG lesions compared to AD and HC, with NMB receptors detectable on some nerve endings. Conclusion: These data show that CNPG does not harbor the strong disease-specific immune activation pathways that are typically found in AD, but is rather characterized by upregulated stromal remodeling mechanisms that might directly impact itch fibers.
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