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Macrophages in inflammatory skin diseases and skin tumors.

作者信息

Liu Si-Han, Zhang Jie, Zuo Ya-Gang

机构信息

Department of Dermatology, State Key Laboratory of Complex Severe and Rare Diseases, National Clinical Research Center for Dermatologic and Immunologic Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

出版信息

Front Immunol. 2024 Dec 5;15:1430825. doi: 10.3389/fimmu.2024.1430825. eCollection 2024.

DOI:10.3389/fimmu.2024.1430825
PMID:39703508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11656021/
Abstract

Macrophages, as specialized, long-lasting phagocytic cells of the innate immune system, have garnered increasing attention due to their wide distribution and various functions. The skin, being the largest immune organ in the human body, presents an intriguing landscape for macrophage research, particularly regarding their roles in inflammatory skin diseases and skin tumors. In this review, we compile the latest research on macrophages in conditions such as atopic dermatitis, psoriasis, systemic sclerosis, systemic lupus erythematosus, rosacea, bullous pemphigoid, melanoma and cutaneous T-cell lymphoma. We aim to contribute to illustrating the pathogenesis and potential new therapies for inflammatory skin diseases and skin tumors from the perspective of macrophages.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5486/11656021/054bceafad19/fimmu-15-1430825-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5486/11656021/b7cadb7ab69c/fimmu-15-1430825-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5486/11656021/cb3f56515a81/fimmu-15-1430825-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5486/11656021/054bceafad19/fimmu-15-1430825-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5486/11656021/b7cadb7ab69c/fimmu-15-1430825-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5486/11656021/cb3f56515a81/fimmu-15-1430825-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5486/11656021/054bceafad19/fimmu-15-1430825-g003.jpg

相似文献

[1]
Macrophages in inflammatory skin diseases and skin tumors.

Front Immunol. 2024-12-5

[2]
Association of the numbers of CD163(+) cells in lesional skin and serum levels of soluble CD163 with disease progression of cutaneous T cell lymphoma.

J Dermatol Sci. 2012-7-27

[3]
Characterization of T-cell subpopulations in skin and peripheral blood of patients with cutaneous T-cell lymphomas and benign inflammatory dermatoses.

J Invest Dermatol. 1983-1

[4]
The Role of Toll-Like Receptors in Skin Host Defense, Psoriasis, and Atopic Dermatitis.

J Immunol Res. 2019-11-14

[5]
Mast cells: novel clinical perspectives from recent insights.

Exp Dermatol. 2009-5

[6]
Exosomes in chronic inflammatory skin diseases and skin tumors.

Exp Dermatol. 2019-3

[7]
The IL-23/IL-17 Pathway in Inflammatory Skin Diseases: From Bench to Bedside.

Front Immunol. 2020

[8]
IL-17 and its role in inflammatory, autoimmune, and oncological skin diseases: state of art.

Int J Dermatol. 2019-10-30

[9]
Thymic Stromal Lymphopoietin in Cutaneous Immune-Mediated Diseases.

Front Immunol. 2021

[10]
Regulatory T cells in inflammatory skin disease: from mice to humans.

Int Immunol. 2019-7-13

引用本文的文献

[1]
Passive physical barrier modulates UVB-induced METosis-related MPO expression and activity, 25-hydroxyvitamin D3-1alpha-hydroxylase, and the shift of tissue-resident macrophages toward M1-associated iNOS.

Front Immunol. 2025-8-14

[2]
Macrophages in rosacea: pathogenesis and therapeutic potential.

Front Immunol. 2025-7-31

本文引用的文献

[1]
Nemolizumab with concomitant topical therapy in adolescents and adults with moderate-to-severe atopic dermatitis (ARCADIA 1 and ARCADIA 2): results from two replicate, double-blind, randomised controlled phase 3 trials.

Lancet. 2024-8-3

[2]
IL-4 and IL-13 are not involved in IL-31-induced itch-associated scratching behaviour in mice.

Exp Dermatol. 2024-6

[3]
MDSC-derived S100A8/9 contributes to lupus pathogenesis by promoting TLR7-mediated activation of macrophages and dendritic cells.

Cell Mol Life Sci. 2024-3-1

[4]
Supercritical CO fluid extract from Stellariae Radix ameliorates 2,4-dinitrochlorobenzene-induced atopic dermatitis by inhibit M1 macrophages polarization via AMPK activation.

Environ Toxicol. 2024-5

[5]
Dictamnine Ameliorates DNFB-Induced Atopic Dermatitis Like Skin Lesions in Mice by Inhibiting M1 Macrophage Polarization and Promoting Autophagy.

Biol Pharm Bull. 2024-1-13

[6]
Mechanism underlying pruritus in recessive dystrophic epidermolysis bullosa: Role of interleukin-31 from mast cells and macrophages.

J Eur Acad Dermatol Venereol. 2024-5

[7]
The nuclear receptor Nurr1 is preferentially expressed in human pro-inflammatory macrophages and limits their inflammatory profile.

Int Immunol. 2024-2-21

[8]
Macrophage autophagy deficiency-induced CEBPB accumulation alleviates atopic dermatitis via impairing M2 polarization.

Cell Rep. 2023-11-28

[9]
ACSL4 inhibition prevents macrophage ferroptosis and alleviates fibrosis in bleomycin-induced systemic sclerosis model.

Arthritis Res Ther. 2023-10-26

[10]
Keratinocyte derived HMGB1 aggravates psoriasis dermatitis via facilitating inflammatory polarization of macrophages and hyperproliferation of keratinocyte.

Mol Immunol. 2023-11

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