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Autoimmunity and Chronic Inflammation - Honorary Special Issue Dedicated to...
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Autoimmunity and Chronic Inflammation - Honorary Special Issue Dedicated to Prof. Dr. Martin Herrmann

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (3 December 2022) | Viewed by 5667

Special Issue Editors

Prof. Dr. Martin Herrmann

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Guest Editor
Department of Medicine 3 – Rheumatology and Immunology, University Clinic Erlangen, Friedrich-Alexander Universität Erlangen-Nürnberg, Universitätsstrasse 25A, 91054 Erlangen, Germany
Interests: clearance deficiency; activation of immune cells; transition from autoimmunity to autoimmune disease
Prof. Dr. Peter Kern

E-Mail Website
Guest Editor
Head of Medical Clinic IV, University Medicine Marburg - Campus Fulda, Pacelliallee 4, 36043 Fulda, Germany
Interests: regulation of inflammation; apoptosis; cell adhesion; antiinflammatory radiotherapy; cytokines
Prof. Dr. Reinhard Voll

E-Mail Website
Guest Editor
Department of Rheumatology and Clinical Immunology, Medical Center—University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg im Breisgau, Germany
Interests: systemic lupus erythematosus; inflammatory diseases; autoimmunity; development of new treatment strategies for autoimmune diseases

Special Issue Information

Dear Colleagues,

This issue deals (I) with the occurrence of cellular and humoral autoimmune responses and with their progression to overt clinical diseases and (II) with the development of chronic inflammation. The main focus of this research topic is on human diseases, but research on pivotal animal models is also welcome. The major sub-topics are (I) the deficient removal or alternative handling of dead and dying cells and their catabolism, (II) clearance deficiency of cell remnants and (aggregated) neutrophil extracellular traps (NETs), (III) tissue destruction due to the chronification of the inflammatory response and persistence of NETs/aggNETs, (IV) the resolution of inflammation, (V) the role of non-immune tissue cells in the induction of autoimmunity, and (VI) the conversion of benign, autoimmune responses into overt clinical diseases. We also encourage the submission of articles dealing with the technology involved in detecting autoimmune and pro-inflammatory immune cells or mediators of autoimmune or inflammatory responses as well as signs of tissue destruction, fibrosis, calcification, vascular occlusion, induced hypoxia, and aberrant bone formation. The description of autoimmune pathologies, their mechanisms, and experimental therapeutic interventions in animal models, as well as therapeutic proposals for humans, are welcome.

Prof. Dr. Martin Herrmann
Prof. Dr. Peter Kern
Prof. Dr. Reinhard Voll
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. Cells is an international peer-reviewed open access semimonthly 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

  • clearance deficiency
  • activation of immune cells
  • transition from autoimmunity to autoimmune disease

Published Papers (2 papers)

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Research

18 pages, 3043 KiB  
Article
Palmitate Inhibits Mouse Macrophage Efferocytosis by Activating an mTORC1-Regulated Rho Kinase 1 Pathway: Therapeutic Implications for the Treatment of Obesity
by László Sós, Éva Garabuczi, Tibor Sághy, Gábor Mocsár and Zsuzsa Szondy
Cells 2022, 11(21), 3502; https://doi.org/10.3390/cells11213502 - 04 Nov 2022
Cited by 1 | Viewed by 2235
Abstract
Every day, billions of our cells die and get cleared without inducing inflammation. When, clearance is improper, uncleared cells undergo secondary necrosis and trigger inflammation. In addition, proper efferocytosis would be required for inducing resolution of inflammation, thus clearance deficiencies in the long [...] Read more.
Every day, billions of our cells die and get cleared without inducing inflammation. When, clearance is improper, uncleared cells undergo secondary necrosis and trigger inflammation. In addition, proper efferocytosis would be required for inducing resolution of inflammation, thus clearance deficiencies in the long term lead to development of various chronic inflammatory diseases. Increasing evidence indicates that obesity, itself being a low-grade inflammatory disease, predisposes to a variety of other chronic inflammatory diseases. Previous studies indicated that this later might be partially related to an impaired efferocytosis induced by increased uptake of circulating saturated fatty acids by macrophages in obese people. Here, we show that palmitate inhibits efferocytosis by bone marrow-derived macrophages in a dose-dependent manner. Palmitate triggers autophagy but also activates an energy-sensing mTORC1/ROCK1 signaling pathway, which interferes with the autophagosome–lysosome fusion, resulting in accumulation of the cellular membranes in autophagosomes. We propose that lack of sufficient plasma membrane supply attenuates efferocytosis of palmitate-exposed macrophages. AMP-activated protein kinase activators lead to mTORC1 inhibition and, consequently, released the palmitate-induced efferocytosis block in macrophages. Thus, they might be useful in the treatment of obesity not only by affecting metabolism thought so far. ROCK1 inhibitors could also be considered. Full article
(This article belongs to the Special Issue Autoimmunity and Chronic Inflammation - Honorary Special Issue Dedicated to Prof. Dr. Martin Herrmann)
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22 pages, 1884 KiB  
Article
Retinoids Promote Mouse Bone Marrow-Derived Macrophage Differentiation and Efferocytosis via Upregulating Bone Morphogenetic Protein-2 and Smad3
by Éva Fige, Zsolt Sarang, László Sós and Zsuzsa Szondy
Cells 2022, 11(18), 2928; https://doi.org/10.3390/cells11182928 - 19 Sep 2022
Cited by 5 | Viewed by 3016
Abstract
Clearance of apoptotic cells by bone marrow-derived macrophages differentiated from monocytes plays a central role in the resolution of inflammation, as the conversion of pro-inflammatory M1 macrophages to M2 macrophages that mediate the resolution process occurs during efferocytosis. Thus, proper efferocytosis is a [...] Read more.
Clearance of apoptotic cells by bone marrow-derived macrophages differentiated from monocytes plays a central role in the resolution of inflammation, as the conversion of pro-inflammatory M1 macrophages to M2 macrophages that mediate the resolution process occurs during efferocytosis. Thus, proper efferocytosis is a prerequisite for proper resolution of inflammation, and failure in efferocytosis is associated with the development of chronic inflammatory diseases. Previous studies from our laboratory have shown that (13R)-all-trans-13,14-dihydroretinol (DHR), the product of retinol saturase, acting from day 4 of monocyte differentiation enhances the efferocytosis capacity of the resulted macrophages. Loss of retinol saturase in mice leads to impaired efferocytosis, and to development of autoimmunity. In the present paper, we report that in differentiating monocytes DHR, retinol, and all-trans retinoic acid all act directly on retinoic acid receptors and enhance the clearance of apoptotic cells by upregulating the expression of several efferocytosis-related genes. The effect of retinoids seems to be mediated by bone morphogenetic protein (BMP)-2, and the Smad3 transcription factor. In addition, retinoids also upregulate the expression of the vitamin D receptor and that of vascular endothelial growth factor A, indicating that altogether retinoids promote the generation of a pro-reparative M2 macrophage population during monocyte differentiation. Full article
(This article belongs to the Special Issue Autoimmunity and Chronic Inflammation - Honorary Special Issue Dedicated to Prof. Dr. Martin Herrmann)
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