Macrophage Pathobiology in Immune-Mediated Inflammatory Disease (IMIDs)

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (25 April 2022) | Viewed by 3710

Special Issue Editors


E-Mail Website
Guest Editor
BioMedX Institute, Im Neunheimer Feld 515, 69120 Heidelberg, Germany
Interests: immune-mediated inflammatory diseases; resolution of inflammation; macrophages; fibroblasts; functional genomics; epigenetics

E-Mail Website
Guest Editor
BioMedX Institute, Im Neunheimer Feld 515, 69120 Heidelberg, Germany
Interests: inflammatory autoimmune diseases; 3D tissue modelling; resolution of inflammation

Special Issue Information

Dear Colleagues, 

In this Special Issue, we are looking for articles that address the functions of blood-derived infiltrating and tissue-resident macrophages in health and autoimmune and inflammatory diseases—in particular, articles that cover the roles of macrophages in chronic inflammation and tissue damage, acute inflammation and other tissue insults, the resolution of inflammation and tissue repair and the switch between inflammation and resolution. These questions can be answered from the perspectives of macrophage ontogeny, tissue-specific phenotypes and functions, macrophage plasticity and memory during chronic inflammation and resolution (in the context of tolerance and trained immunity) and epigenetics. We invite articles from diverse fields with strong macrophage biology research, including, but not restricted to, the following:

  1. Diseases of the nervous system: multiple sclerosis, neuromyelitis optica, myasthenia gravis, et cetera.
  2. Diseases of the intestine: inflammatory bowel disease, celiac disease.
  3. Diseases of the skin: atopic dermatitis, psoriasis, aberrant wound healing.
  4. Diseases of the joint: rheumatoid arthritis, psoriatic arthritis, osteoarthritis.
  5. Systemic lupus erythematosus, systemic sclerosis, age-related chronic inflammatory diseases, et cetera.
  6. Vascular inflammatory diseases: atherosclerosis and vasculitides.

Dr. Mojca Frank-Bertoncelj
Dr. Swathi Lingam
Guest Editors

Manuscript Submission Information

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Keywords

  • macrophage pathobiology
  • immune-mediated inflammatory diseases
  • acute and chronic inflammation
  • tissue damage
  • resolution of inflammation

Published Papers (1 paper)

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Research

18 pages, 7105 KiB  
Article
miR-185-5p Regulates Inflammation and Phagocytosis through CDC42/JNK Pathway in Macrophages
by Xirui Ma, Huifang Liu, Jing Zhu, Caoxu Zhang, Yajie Peng, Ziming Mao, Yu Jing and Fengling Chen
Genes 2022, 13(3), 468; https://doi.org/10.3390/genes13030468 - 7 Mar 2022
Cited by 16 | Viewed by 3185
Abstract
Macrophage activation is an essential component of systemic chronic inflammation and chronic inflammatory diseases. Emerging evidence implicates miR-185-5p in chronic inflammation diseases. However, the regulatory role of miR-185-5p in macrophage pro-inflammatory activation has not been studied previously. Here, we identified that miR-185-5p was [...] Read more.
Macrophage activation is an essential component of systemic chronic inflammation and chronic inflammatory diseases. Emerging evidence implicates miR-185-5p in chronic inflammation diseases. However, the regulatory role of miR-185-5p in macrophage pro-inflammatory activation has not been studied previously. Here, we identified that miR-185-5p was one of the top genes and effectively downregulated in two macrophage miRNA expression datasets from GEO. Under LPS stress, miR-185-5p overexpression reduced pro-inflammatory cytokine expression, suppressed phagocytosis in RAW264.7 macrophage. miR-185-5p inhibitors augmented pro-inflammatory effects of LPS in macrophage. Mechanically, miR-185-5p sponged and negatively regulated the protein expression of CDC42. Ablation of CDC42 with selective CDC42 inhibitor CASIN reversed the pro-inflammatory effect of miR-185-5p inhibitors through inhibiting MAPK/JNK pathways. Collectively, these data demonstrate that miR-185-5p exhibited anti-inflammatory functions in LPS-induced RAW264.7 macrophages at least partially through CDC42/JNK pathways. Our findings yield insights into the understanding of miR-185-5p-regulated network in macrophages inflammation, which is beneficial for exploring miRNA-protein interaction in atherosclerotic inflammation. Full article
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