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Biology
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Activation of Macrophages
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Activation of Macrophages

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 8704

Special Issue Editor

Dr. Jingbo Pang

E-Mail Website
Guest Editor
Center for Wound Healing and Tissue Regeneration, Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL 60612, USA
Interests: macrophages; monocytes; wound healing; diabetes; adipose tissue; inflammation; macrophage/monocyte heterogeneity

Special Issue Information

Dear Colleagues,

Macrophages, a key component of the innate immunity, fulfill numerous tasks in diverse biological processes, ranging from the early initiation and amplification of inflammatory cascades to the late phagocytosis and clearance of cell debris, invading microorganisms and other foreign substances. The activation of macrophages is a complex procedure mediated by various types of factors, including signals from cytokines, PAMPs, DAMPs and other secreted products. Macrophages exhibit a high degree of plasticity, and their metabolism/functions are tightly associated with different activation phenotypes. In addition to the widely used M1 vs. M2 classification scheme, the recent progress and development of new experimental approaches such as mass cytometry, spectral flow cytometry, and scRNAseq have greatly expanded the understanding of macrophage phenotypes under different pathophysiological conditions; however, much remains to be explored.

In this Special Issue, we will collect the latest advances in macrophage activation research. We welcome research focusing on macrophage heterogeneity, the coordination of environmental, pathogenic signals and cell intrinsic factors modulating activation of macrophages, as well as changes in response to macrophage activation and polarization in an array of pathophysiological processes and diseases. As such, original research articles and reviews are welcome.

We look forward to receiving your contributions.

Dr. Jingbo Pang
Guest Editor

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. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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
  • monocytes
  • inflammation
  • cytokines
  • chemokines
  • danger signals
  • tissue repair
  • antigen-presenting cells
  • metabolism

Published Papers (4 papers)

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Research

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20 pages, 3131 KiB  
Article
sTREM2 Differentially Affects Cytokine Expression in Myeloid-Derived Cell Models via MAPK–JNK Signaling Pathway
by Ryan Arsenault, Steven Marshall, Patrick Salois, Qiao Li and Wandong Zhang
Biology 2024, 13(2), 87; https://doi.org/10.3390/biology13020087 - 30 Jan 2024
Viewed by 1438
Abstract
TREM2 is a critical innate immune receptor primarily expressed on myeloid-derived cells, such as microglia and macrophages. Mutations in TREM2 are linked to several neurodegenerative diseases including Alzheimer’s disease (AD). TREM2 can be cleaved from the cell membrane and released as soluble TREM2 [...] Read more.
TREM2 is a critical innate immune receptor primarily expressed on myeloid-derived cells, such as microglia and macrophages. Mutations in TREM2 are linked to several neurodegenerative diseases including Alzheimer’s disease (AD). TREM2 can be cleaved from the cell membrane and released as soluble TREM2 (sTREM2). sTREM2 levels are shown to peak prior to AD, with its levels fluctuating throughout disease progression. However, the mechanism by which sTREM2 may affect innate immune responses is largely uncharacterized. In this study, we investigated whether sTREM2 can induce inflammatory response in myeloid-derived THP-1 monocytes and macrophages and characterized the signaling mechanisms involved. Our results show that sTREM2 was capable of stimulating the expression of several inflammatory cytokines in THP-1 cells throughout the time course of 2 h to 8 h but inducing anti-inflammatory cytokine expression at later time points. A TREM2 antibody was capable of inhibiting the expression of some cytokines induced by sTREM2 but enhancing others. The complex of sTREM2/TREM2 antibody was shown to enhance IL-1β expression, which was partially blocked by an NLRP3 specific inhibitor, indicating that the complex activated the NRLP3 inflammasome pathway. sTREM2 was also shown to have differential effects on cytokine expression in M0, M1, and M2 macrophages differentiated from THP-1 cells. sTREM2 has a more stimulating effect on cytokine expression in M0 macrophages, less of an effect on M2 macrophages, and some inhibitory effects on cytokine expression in M1 macrophages at early time points. Analyses of several signaling pathways revealed that sTREM2-induced expression of cytokines occurs mainly through MAPK–JNK signaling. Our work reveals differential effects of sTREM2 on cytokine expression profiles of THP-1 cells and macrophages and demonstrates that the MAPK–JNK signaling pathway is mainly responsible for sTREM2-induced cytokine expression. Full article
(This article belongs to the Special Issue Activation of Macrophages)
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17 pages, 5551 KiB  
Article
Effective Reversal of Macrophage Polarization by Inhibitory Combinations Predicted by a Boolean Protein–Protein Interaction Model
by Gabor Szegvari, David Dora and Zoltan Lohinai
Biology 2023, 12(3), 376; https://doi.org/10.3390/biology12030376 - 27 Feb 2023
Cited by 1 | Viewed by 1749
Abstract
Background: The function and polarization of macrophages has a significant impact on the outcome of many diseases. Targeting tumor-associated macrophages (TAMs) is among the greatest challenges to solve because of the low in vitro reproducibility of the heterogeneous tumor microenvironment (TME). To create [...] Read more.
Background: The function and polarization of macrophages has a significant impact on the outcome of many diseases. Targeting tumor-associated macrophages (TAMs) is among the greatest challenges to solve because of the low in vitro reproducibility of the heterogeneous tumor microenvironment (TME). To create a more comprehensive model and to understand the inner workings of the macrophage and its dependence on extracellular signals driving polarization, we propose an in silico approach. Methods: A Boolean control network was built based on systematic manual curation of the scientific literature to model the early response events of macrophages by connecting extracellular signals (input) with gene transcription (output). The network consists of 106 nodes, classified as 9 input, 75 inner and 22 output nodes, that are connected by 217 edges. The direction and polarity of edges were manually verified and only included in the model if the literature plainly supported these parameters. Single or combinatory inhibitions were simulated mimicking therapeutic interventions, and output patterns were analyzed to interpret changes in polarization and cell function. Results: We show that inhibiting a single target is inadequate to modify an established polarization, and that in combination therapy, inhibiting numerous targets with individually small effects is frequently required. Our findings show the importance of JAK1, JAK3 and STAT6, and to a lesser extent STK4, Sp1 and Tyk2, in establishing an M1-like pro-inflammatory polarization, and NFAT5 in creating an anti-inflammatory M2-like phenotype. Conclusions: Here, we demonstrate a protein–protein interaction (PPI) network modeling the intracellular signalization driving macrophage polarization, offering the possibility of therapeutic repolarization and demonstrating evidence for multi-target methods. Full article
(This article belongs to the Special Issue Activation of Macrophages)
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Review

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17 pages, 1493 KiB  
Review
Unraveling the Immune Microenvironment in Classic Hodgkin Lymphoma: Prognostic and Therapeutic Implications
by Vasileios Georgoulis, Alexandra Papoudou-Bai, Alexandros Makis, Panagiotis Kanavaros and Eleftheria Hatzimichael
Biology 2023, 12(6), 862; https://doi.org/10.3390/biology12060862 - 15 Jun 2023
Cited by 2 | Viewed by 2183
Abstract
Classic Hodgkin lymphoma (cHL) is a lymphoid neoplasm composed of rare neoplastic Hodgkin and Reed–Sternberg (HRS) cells surrounded by a reactive tumor microenvironment (TME) with suppressive properties against anti-tumor immunity. TME is mainly composed of T cells (CD4 helper, CD8 cytotoxic and regulatory) [...] Read more.
Classic Hodgkin lymphoma (cHL) is a lymphoid neoplasm composed of rare neoplastic Hodgkin and Reed–Sternberg (HRS) cells surrounded by a reactive tumor microenvironment (TME) with suppressive properties against anti-tumor immunity. TME is mainly composed of T cells (CD4 helper, CD8 cytotoxic and regulatory) and tumor-associated macrophages (TAMs), but the impact of these cells on the natural course of the disease is not absolutely understood. TME contributes to the immune evasion of neoplastic HRS cells through the production of various cytokines and/or the aberrant expression of immune checkpoint molecules in ways that have not been fully understood yet. Herein, we present a comprehensive review of findings regarding the cellular components and the molecular features of the immune TME in cHL, its correlation with treatment response and prognosis, as well as the potential targeting of the TME with novel therapies. Among all cells, macrophages appear to be a most appealing target for immunomodulatory therapies, based on their functional plasticity and antitumor potency. Full article
(This article belongs to the Special Issue Activation of Macrophages)
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24 pages, 1450 KiB  
Review
AIF1: Function and Connection with Inflammatory Diseases
by Diego De Leon-Oliva, Cielo Garcia-Montero, Oscar Fraile-Martinez, Diego Liviu Boaru, Luis García-Puente, Antonio Rios-Parra, Maria J. Garrido-Gil, Carlos Casanova-Martín, Natalio García-Honduvilla, Julia Bujan, Luis G. Guijarro, Melchor Alvarez-Mon and Miguel A. Ortega
Biology 2023, 12(5), 694; https://doi.org/10.3390/biology12050694 - 9 May 2023
Cited by 9 | Viewed by 2857
Abstract
Macrophages are a type of immune cell distributed throughout all tissues of an organism. Allograft inflammatory factor 1 (AIF1) is a calcium-binding protein linked to the activation of macrophages. AIF1 is a key intracellular signaling molecule that participates in phagocytosis, membrane ruffling and [...] Read more.
Macrophages are a type of immune cell distributed throughout all tissues of an organism. Allograft inflammatory factor 1 (AIF1) is a calcium-binding protein linked to the activation of macrophages. AIF1 is a key intracellular signaling molecule that participates in phagocytosis, membrane ruffling and F-actin polymerization. Moreover, it has several cell type-specific functions. AIF1 plays important roles in the development of several diseases: kidney disease, rheumatoid arthritis, cancer, cardiovascular diseases, metabolic diseases and neurological disorders, and in transplants. In this review, we present a comprehensive review of the known structure, functions and role of AIF1 in inflammatory diseases. Full article
(This article belongs to the Special Issue Activation of Macrophages)
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