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TSLP 和 IL-1β 在皮肤过敏致敏和特应性进展中的上下文相关功能。

Context-dependent function of TSLP and IL-1β in skin allergic sensitization and atopic march.

机构信息

Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS UMR 7104 - Inserm U 1258 - Université de Strasbourg, Illkirch, France.

CNRS-Strasbourg University, UAR3286, Plate-Forme de Chimie Biologique Intégrative de Strasbourg/Strasbourg Drug Discovery and Development Institute, ESBS, Illkirch, France.

出版信息

Nat Commun. 2022 Sep 1;13(1):4703. doi: 10.1038/s41467-022-32196-1.

DOI:10.1038/s41467-022-32196-1
PMID:36050303
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9437001/
Abstract

Atopic diseases, including atopic dermatitis (AD) and asthma, affect a large proportion of the population, with increasing prevalence worldwide. AD often precedes the development of asthma, known as the atopic march. Allergen sensitization developed through the barrier-defective skin of AD has been recognized to be a critical step leading to asthma, in which thymic stromal lymphopoietin (TSLP) was previously shown to be critical. In this study, using a laser-assistant microporation system to disrupt targeted skin layers for generating micropores at a precise anatomic depth of mouse skin, we model allergen exposure superficially or deeply in the skin, leading to epicutaneous sensitization or dermacutaneous sensitization that is associated with a different cytokine microenvironment. Our work shows a differential requirement for TSLP in these two contexts, and identifies an important function for IL-1β, which is independent of TSLP, in promoting allergen sensitization and subsequent allergic asthma.

摘要

特应性疾病，包括特应性皮炎（AD）和哮喘，影响了很大一部分人群，其在全球的患病率呈上升趋势。AD 常先于哮喘发生，被称为特应性进程。通过 AD 受损的皮肤发生的过敏原致敏已被认为是导致哮喘的关键步骤，此前已证实胸腺基质淋巴细胞生成素（TSLP）在此过程中起关键作用。在这项研究中，我们使用激光辅助微穿孔系统破坏靶向皮肤层，在小鼠皮肤的精确解剖深度产生微孔，从而在皮肤的浅层或深层模拟过敏原暴露，导致经皮致敏或真皮致敏，这与不同的细胞因子微环境相关。我们的工作表明，在这两种情况下 TSLP 的需求存在差异，并确定了白细胞介素-1β（IL-1β）的一个重要功能，它独立于 TSLP，可促进过敏原致敏和随后的过敏性哮喘。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/9772e496c287/41467_2022_32196_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/51dbb9c09c32/41467_2022_32196_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/2e01bf4b53a7/41467_2022_32196_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/cb9f91590839/41467_2022_32196_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/9d393d93a15d/41467_2022_32196_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/b3c1e7acdfdc/41467_2022_32196_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/9772e496c287/41467_2022_32196_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/51dbb9c09c32/41467_2022_32196_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/54cc24c125fe/41467_2022_32196_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/7306e17bb5fa/41467_2022_32196_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/2e01bf4b53a7/41467_2022_32196_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/cb9f91590839/41467_2022_32196_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/9d393d93a15d/41467_2022_32196_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/b3c1e7acdfdc/41467_2022_32196_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a57/9437001/9772e496c287/41467_2022_32196_Fig8_HTML.jpg

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