文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期,新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2025

钙/钙调蛋白依赖性蛋白激酶 IV 通过小鼠巨噬细胞和角质形成细胞促进咪喹莫特诱导的银屑病炎症。

Calcium/calmodulin-dependent protein kinase IV promotes imiquimod-induced psoriatic inflammation via macrophages and keratinocytes in mice.

机构信息

Department of Dermatology, the First Affiliated Hospital of Anhui Medical University, Hefei, China.

Institute of Dermatology, Anhui Medical University, Hefei, China.

出版信息

Nat Commun. 2022 Jul 22;13(1):4255. doi: 10.1038/s41467-022-31935-8.


DOI:10.1038/s41467-022-31935-8
PMID:35869084
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9307837/
Abstract

CaMK4 has an important function in autoimmune diseases, and the contribution of CaMK4 in psoriasis remains obscure. Here, we show that CaMK4 expression is significantly increased in psoriatic lesional skin from psoriasis patients compared to healthy human skin as well as inflamed skin from an imiquimod (IMQ)-induced mouse model of psoriasis compared to healthy mouse skin. Camk4-deficient (Camk4) mice treated with IMQ exhibit reduced severity of psoriasis compared to wild-type (WT) mice. There are more macrophages and fewer IL-17Aγδ TCR cells in the skin of IMQ-treated Camk4 mice compared to IMQ-treated WT mice. CaMK4 inhibits IL-10 production by macrophages, thus allowing excessive psoriatic inflammation. Deletion of Camk4 in macrophages alleviates IMQ-induced psoriatic inflammation in mice. In keratinocytes, CaMK4 inhibits apoptosis as well as promotes cell proliferation and the expression of pro-inflammatory genes such as S100A8 and CAMP. Taken together, these data indicate that CaMK4 regulates IMQ-induced psoriasis by sustaining inflammation and provides a potential target for psoriasis treatment.

摘要

钙调蛋白依赖性蛋白激酶 4(CaMK4)在自身免疫性疾病中具有重要作用,但其在银屑病中的作用尚不清楚。本研究表明,与健康人皮肤相比,银屑病患者皮损皮肤以及咪喹莫特(IMQ)诱导的银屑病样小鼠模型的炎症皮肤中 CaMK4 的表达显著增加。与野生型(WT)小鼠相比,用 IMQ 处理的 Camk4 缺陷(Camk4)小鼠银屑病的严重程度降低。与 IMQ 处理的 WT 小鼠相比,IMQ 处理的 Camk4 小鼠皮肤中的巨噬细胞增多,而白细胞介素 17AγδT 细胞(IL-17AγδTCR 细胞)减少。CaMK4 抑制巨噬细胞中白细胞介素 10(IL-10)的产生,从而导致过度的银屑病炎症。在巨噬细胞中删除 Camk4 可减轻 IMQ 诱导的小鼠银屑病炎症。在角质形成细胞中,CaMK4 抑制细胞凋亡,促进细胞增殖和促炎基因(如 S100A8 和 CAMP)的表达。总之,这些数据表明 CaMK4 通过维持炎症来调节 IMQ 诱导的银屑病,并为银屑病的治疗提供了一个潜在的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/1542c1fd99ad/41467_2022_31935_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/68198a5d2c0d/41467_2022_31935_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/75b35cc00a7c/41467_2022_31935_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/65d47bea9bad/41467_2022_31935_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/d863fc9e530b/41467_2022_31935_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/eb064a2b59e6/41467_2022_31935_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/f86472510be5/41467_2022_31935_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/de2a514e9656/41467_2022_31935_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/3793b5d25900/41467_2022_31935_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/ee012b13638a/41467_2022_31935_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/1542c1fd99ad/41467_2022_31935_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/68198a5d2c0d/41467_2022_31935_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/75b35cc00a7c/41467_2022_31935_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/65d47bea9bad/41467_2022_31935_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/d863fc9e530b/41467_2022_31935_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/eb064a2b59e6/41467_2022_31935_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/f86472510be5/41467_2022_31935_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/de2a514e9656/41467_2022_31935_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/3793b5d25900/41467_2022_31935_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/ee012b13638a/41467_2022_31935_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3496/9307837/1542c1fd99ad/41467_2022_31935_Fig10_HTML.jpg

相似文献

[1]
Calcium/calmodulin-dependent protein kinase IV promotes imiquimod-induced psoriatic inflammation via macrophages and keratinocytes in mice.

Nat Commun. 2022-7-22

[2]
IRF-2 haploinsufficiency causes enhanced imiquimod-induced psoriasis-like skin inflammation.

J Dermatol Sci. 2017-12-28

[3]
Anoctamin1 Induces Hyperproliferation of HaCaT Keratinocytes and Triggers Imiquimod-Induced Psoriasis-Like Skin Injury in Mice.

Int J Mol Sci. 2021-7-1

[4]
Indirubin ameliorates imiquimod-induced psoriasis-like skin lesions in mice by inhibiting inflammatory responses mediated by IL-17A-producing γδ T cells.

Mol Immunol. 2018-7-29

[5]
Unconjugated bilirubin and its derivative ameliorate IMQ-induced psoriasis-like skin inflammation in mice by inhibiting MMP9 and MAPK pathway.

Int Immunopharmacol. 2024-3-30

[6]
Losartan ointment attenuates imiquimod-induced psoriasis-like inflammation.

Int Immunopharmacol. 2021-11

[7]
Interleukin-18 exacerbates skin inflammation and affects microabscesses and scale formation in a mouse model of imiquimod-induced psoriasis.

Chin Med J (Engl). 2019-3-20

[8]
Leptin deficiency in mice counteracts imiquimod (IMQ)-induced psoriasis-like skin inflammation while leptin stimulation induces inflammation in human keratinocytes.

Exp Dermatol. 2017-4

[9]
Interleukin-38 overexpression in keratinocytes limits desquamation but does not affect the global severity of imiquimod-induced skin inflammation in mice.

Front Immunol. 2024

[10]
IL-23/IL-17 immune axis mediates the imiquimod-induced psoriatic inflammation by activating ACT1/TRAF6/TAK1/NF-κB pathway in macrophages and keratinocytes.

Kaohsiung J Med Sci. 2023-8

引用本文的文献

[1]
An Immunomodulating Peptide with Potential to Promote Anticancer Immunity Without Compromising Immune Tolerance.

Biomedicines. 2025-8-5

[2]
Impact of serum calcium levels on the occurrence of sepsis and prognosis in hospitalized patients with concomitant psoriasis: a retrospective study based on the MIMIC-IV database.

Front Immunol. 2025-7-22

[3]
Integrated Multi-Omics Profiling Reveals That Highly Pyroptotic MDMs Contribute to Psoriasis Progression Through CXCL16.

Biomedicines. 2025-7-18

[4]
Antisense oligonucleotides targeting IRF4 alleviate psoriasis.

Acta Pharm Sin B. 2025-7

[5]
Targeting KAT8 alleviates self-RNA-driven skin inflammation by modulating histone H4 lysine 16 acetylation in psoriasis.

Cell Death Differ. 2025-7-21

[6]
Decoding Macrophage Dynamics: A Pathway to Understanding and Treating Inflammatory Skin Diseases.

Int J Mol Sci. 2025-5-1

[7]
Age and Sex Effects on Blood Retrotransposable Element Expression Levels: Findings From the Population-Based Rhineland Study.

Aging Cell. 2025-8

[8]
Quantitative Proteomic Analysis Indicates That Pggt1b Deficiency Promotes Cytokine Secretion in Resiquimod-Stimulated Bone Marrow-Derived Macrophages via the NF-κB Pathway.

Immun Inflamm Dis. 2025-4

[9]
Histone Modifications and DNA Methylation in Psoriasis: A Cellular Perspective.

Clin Rev Allergy Immunol. 2025-1-27

[10]
Engineered Mesenchymal Stem Cell-Derived Extracellular Vesicles Scavenge Self-Antigens for Psoriasis Therapy via Modulating Metabolic and Immunological Disorders.

Adv Sci (Weinh). 2025-2

本文引用的文献

[1]
Analysis of Myeloid Cells in Mouse Tissues with Flow Cytometry.

STAR Protoc. 2020-6-19

[2]
4-1BBL Regulates the Polarization of Macrophages, and Inhibition of 4-1BBL Signaling Alleviates Imiquimod-Induced Psoriasis.

J Immunol. 2020-2-10

[3]
BMP7 aberrantly induced in the psoriatic epidermis instructs inflammation-associated Langerhans cells.

J Allergy Clin Immunol. 2020-4

[4]
Biology and therapeutic potential of interleukin-10.

J Exp Med. 2020-1-6

[5]
Pyruvate kinase M2 is requisite for Th1 and Th17 differentiation.

JCI Insight. 2019-6-20

[6]
B1 cells protect against Schistosoma japonicum-induced liver inflammation and fibrosis by controlling monocyte infiltration.

PLoS Negl Trop Dis. 2019-6-13

[7]
The Healing Power of Neutrophils.

Trends Immunol. 2019-5-31

[8]
Nonclassical Monocytes in Health and Disease.

Annu Rev Immunol. 2019-4-26

[9]
IL-10 Family Cytokines IL-10 and IL-22: from Basic Science to Clinical Translation.

Immunity. 2019-4-16

[10]
The role of regulatory T cells and anti-inflammatory cytokines in psoriasis.

Acta Dermatovenerol Alp Pannonica Adriat. 2018-3

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索