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Immune Modulation of Macrophages: 2nd Edition
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Immune Modulation of Macrophages: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 1789

Special Issue Editors

Prof. Dr. Paul Kwong Hang Tam

E-Mail Website
Guest Editor
1. Faculty of Medicine, Macau University of Science and Technology, Macau SAR, China
2. Department of Surgery, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
Interests: genetics and development biology of birth defects; genomics of childhood tumors; immunology and inflammation
Special Issues, Collections and Topics in MDPI journals
Dr. Yan Chen

E-Mail Website
Guest Editor
1. Faculty of Medicine, Macau University of Science and Technology, Macau SAR, China
2. Department of Surgery, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
Interests: immunology and inflammation in birth defects and tumors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

A macrophage is a multifunctional cell type presenting consistent phenotype changes over its lifespan beginning from the embryonic period. The differentiation and maturation dependent on the microenvironment and in response to the internal and external stimuli often result in the heterogenicity of the cells, by which the interpretation of the function becomes difficult. As a result, therapeutic treatment in cell targeting has frequently been ineffective. With the increased knowledge provided by updated forms of technology, especially multi-omics and spatial transcriptomic technologies, the functional understanding of macrophages in both physiological and pathological conditions in different tissues and organs is becoming increasingly advanced. In line with the creation of new technologies, the modulation of the cells in different pathological conditions, such as cancer, in response to the different drugs or reagents for different diseases during the development stages will provide a novel phenotypical assessment. A good understanding of the alternating functions of macrophages will help scientists to develop new strategies in terms of precision or personalized therapies in treating diseases.

This Special Issue entitled “Immune Modulation of Macrophages 2.0” invites submissions of original reviews in this field of research, and focuses on the advanced technology concerning the understanding of the heterogenicity of cells in the disease process, especially in the phenotype changes and pathway analysis in response to the external treatment in disease treatments.

Prof. Dr. Paul Kwong Hang Tam
Dr. Yan Chen
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • macrophages
  • treatment
  • phenotype change
  • pathway analysis

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Published Papers (2 papers)

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Research

12 pages, 3657 KiB  
Article
Ginsenoside Rh2 Alleviates LPS-Induced Inflammatory Responses by Binding to TLR4/MD-2 and Blocking TLR4 Dimerization
by Shujuan Pan, Luyuan Peng, Qion Yi, Weijin Qi, Hui Yang, Hongying Wang and Lu Wang
Int. J. Mol. Sci. 2024, 25(17), 9546; https://doi.org/10.3390/ijms25179546 - 2 Sep 2024
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Abstract
Lipopolysaccharide (LPS) triggers a severe systemic inflammatory reaction in mammals, with the dimerization of TLR4/MD-2 upon LPS stimulation serving as the pivotal mechanism in the transmission of inflammatory signals. Ginsenoside Rh2 (G-Rh2), one of the active constituents of [...] Read more.
Lipopolysaccharide (LPS) triggers a severe systemic inflammatory reaction in mammals, with the dimerization of TLR4/MD-2 upon LPS stimulation serving as the pivotal mechanism in the transmission of inflammatory signals. Ginsenoside Rh2 (G-Rh2), one of the active constituents of red ginseng, exerts potent anti-inflammatory activity. However, whether G-Rh2 can block the TLR4 dimerization to exert anti-inflammatory effects remains unclear. Here, we first investigated the non-cytotoxic concentration of G-Rh2 on RAW 264.7 cells, and detected the releases of pro-inflammatory cytokines in LPS-treated RAW 264.7 cells, and then uncovered the mechanisms involved in the anti-inflammatory activity of G-Rh2 through flow cytometry, fluorescent membrane localization, Western blotting, co-immunoprecipitation (Co-IP), molecular docking and surface plasmon resonance (SPR) analysis in LPS-stimulated macrophages. Our results show that G-Rh2 stimulation markedly inhibited the secretion of LPS-induced interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and nitric oxide (NO). Additionally, G-Rh2 blocked the binding of LPS with the membrane of RAW 264.7 cells through direct interaction with TLR4 and MD-2 proteins, leading to the disruption of the dimerization of TLR4 and MD-2, followed by suppression of the TLR4/NF-κB signaling pathway. Our results suggest that G-Rh2 acts as a new inhibitor of TLR4 dimerization and may serve as a promising therapeutic agent against inflammation. Full article
(This article belongs to the Special Issue Immune Modulation of Macrophages: 2nd Edition)
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19 pages, 24940 KiB  
Article
LHFPL2 Serves as a Potential Biomarker for M2 Polarization of Macrophages in Renal Cell Carcinoma
by Xiaocheng Gong, Yunfei Liu, Qian Zhang, Keying Liang, Jinfen Wei and Hongli Du
Int. J. Mol. Sci. 2024, 25(12), 6707; https://doi.org/10.3390/ijms25126707 - 18 Jun 2024
Viewed by 922
Abstract
Renal cell carcinoma (RCC) is one of the most common malignant tumors of the kidney, presenting significant challenges for clinical diagnosis and treatment. Macrophages play crucial roles in RCC, promoting tumor progression and warranting further investigation. Previous studies have identified LHFPL2 as a [...] Read more.
Renal cell carcinoma (RCC) is one of the most common malignant tumors of the kidney, presenting significant challenges for clinical diagnosis and treatment. Macrophages play crucial roles in RCC, promoting tumor progression and warranting further investigation. Previous studies have identified LHFPL2 as a transmembrane protein associated with reproduction, but its relationship with tumors or macrophages has not been discussed. This study utilized transcriptomic sequencing data from 609 KIRC patients in the TCGA database and single-cell sequencing data from 34,326 renal carcinoma cells for subsequent analysis. We comprehensively evaluated the expression of LHFPL2 and its relationship with clinical features, tumor prognosis, immune infiltration, and mutations. Additionally, we further assessed the correlation between LHFPL2 and macrophage M2 polarization using single-cell data and explored its potential as a cancer therapeutic target through molecular docking. The results demonstrated that LHFPL2 is upregulated in RCC and associated with poor survival rates. In clinical staging, the proportion of malignant and high-metastasis patients was higher in the high-LHFPL2 group than in the low-LHFPL2 group. Furthermore, we found that LHFPL2 influences RCC immune infiltration, with its expression positively correlated with various immune checkpoint and M2-related gene expressions, positively associated with M2 macrophage infiltration, and negatively correlated with activated NK cells. Moreover, LHFPL2 showed specific expression in macrophages, with the high-expression subgroup exhibiting higher M2 polarization, hypoxia, immune evasion, and angiogenesis scores, promoting tumor progression. Finally, we predicted several potential drugs targeting LHFPL2, such as conivaptan and nilotinib. Our analysis elaborately delineates the immune characteristics of LHFPL2 in the tumor microenvironment and its positive correlation with macrophage M2 polarization, providing new insights into tumor immunotherapy. We also propose potential FDA-approved drugs targeting this gene, which should be tested for their binding effects with LHFPL2 in future studies. Full article
(This article belongs to the Special Issue Immune Modulation of Macrophages: 2nd Edition)
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