巨噬细胞极化在炎症性免疫性皮肤病中的研究进展。

IF 4.4 3区 医学 Q2 IMMUNOLOGY
Tingting Xia, Shengping Fu, Ruilin Yang, Kang Yang, Wei Lei, Ying Yang, Qian Zhang, Yujie Zhao, Jiang Yu, Limei Yu, Tao Zhang
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引用次数: 1

摘要

当暴露于各种微环境刺激时,巨噬细胞具有高度可塑性,并主要分化为促炎性M1型和抗炎性M2型,这两种类型几乎都具有完全相反的功能。由于这一特点,巨噬细胞在免疫和炎症的不同阶段发挥着不同的功能。炎症性免疫性皮肤病通常表现为M1/M2巨噬细胞比例失衡,改变巨噬细胞极化表型可能会使症状恶化或好转。因此,本文综述了巨噬细胞极化机制、炎症相关信号通路(JAK/STAT、NF-κB和PI3K/Akt),以及两者在炎症免疫性皮肤病(银屑病、AD、SLE、BD等)中的作用,为相关疾病的基础和临床研究提供了新的方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Advances in the study of macrophage polarization in inflammatory immune skin diseases.

Advances in the study of macrophage polarization in inflammatory immune skin diseases.

Advances in the study of macrophage polarization in inflammatory immune skin diseases.

When exposed to various microenvironmental stimuli, macrophages are highly plastic and primarily polarized into the pro-inflammatory M1-type and the anti-inflammatory M2-type, both of which perform almost entirely opposing functions. Due to this characteristic, macrophages perform different functions at different stages of immunity and inflammation. Inflammatory immune skin diseases usually show an imbalance in the M1/M2 macrophage ratio, and altering the macrophage polarization phenotype can either make the symptoms worse or better. Therefore, this review presents the mechanisms of macrophage polarization, inflammation-related signaling pathways (JAK/STAT, NF-κB, and PI3K/Akt), and the role of both in inflammatory immune skin diseases (psoriasis, AD, SLE, BD, etc.) to provide new directions for basic and clinical research of related diseases.

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来源期刊
CiteScore
7.90
自引率
0.00%
发文量
18
审稿时长
>12 weeks
期刊介绍: Journal of Inflammation welcomes research submissions on all aspects of inflammation. The five classical symptoms of inflammation, namely redness (rubor), swelling (tumour), heat (calor), pain (dolor) and loss of function (functio laesa), are only part of the story. The term inflammation is taken to include the full range of underlying cellular and molecular mechanisms involved, not only in the production of the inflammatory responses but, more importantly in clinical terms, in the healing process as well. Thus the journal covers molecular, cellular, animal and clinical studies, and related aspects of pharmacology, such as anti-inflammatory drug development, trials and therapeutic developments. It also considers publication of negative findings. Journal of Inflammation aims to become the leading online journal on inflammation and, as online journals replace printed ones over the next decade, the main open access inflammation journal. Open access guarantees a larger audience, and thus impact, than any restricted access equivalent, and increasingly so, as the escalating costs of printed journals puts them outside University budgets. The unrestricted access to research findings in inflammation aids in promoting dynamic and productive dialogue between industrial and academic members of the inflammation research community, which plays such an important part in the development of future generations of anti-inflammatory therapies.
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