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Biomedicines
Special Issues
Inflammation and Immunosenescence in Age-Related Diseases
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Inflammation and Immunosenescence in Age-Related Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 5271

Special Issue Editors

Dr. Luca Pangrazzi

E-Mail Website
Guest Editor
Institute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria
Interests: investigating immune dysfunction; pro-inflammatory changes and immunosenescence during aging
Special Issues, Collections and Topics in MDPI journals
Dr. Magdalena Hagen

E-Mail Website
Guest Editor
Institute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria
Interests: vaccinations and immunosenescence in humans

Special Issue Information

Dear Colleagues,

Aging is accompanied by the decreased efficacy of the immune system. This has commonly been associated with reduced responses to vaccinations and increased mortality in the elderly. This process is known as immunosenescence, and it affects both innate and adaptive immunity. Age-related inflammation ("inflammaging) plays a determinant role in immunosenescence, and it therefore contributes to the pathogenesis of chronic diseases. The aim of this Special Issue is to decipher the role of inflammation and immunosenescence in age-related diseases. Original papers or reviews aiming at describing the interplay between immune dysfunction, inflammation, and immunosenescence in age-related diseases are welcome for this Special Issue.

Dr. Luca Pangrazzi
Dr. Magdalena Hagen
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. Biomedicines 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 2600 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

  • immunology
  • aging
  • inflammation
  • senescence
  • immunosenescence

Published Papers (3 papers)

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Research

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17 pages, 1905 KiB  
Article
The Activation of JAK/STAT3 Signaling and the Complement System Modulate Inflammation in the Primary Human Dermal Fibroblasts of PXE Patients
by Christopher Lindenkamp, Ricarda Plümers, Michel R. Osterhage, Olivier M. Vanakker, Judith Van Wynsberghe, Cornelius Knabbe and Doris Hendig
Biomedicines 2023, 11(10), 2673; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11102673 - 29 Sep 2023
Cited by 1 | Viewed by 1008
Abstract
Previous studies revealed a link between inflammation and overactivation of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling in syndromes associated with aging. Pseudoxanthoma elasticum (PXE), a rare autosomal-recessive disorder, arises from mutations in ATP-binding cassette subfamily C member 6 [...] Read more.
Previous studies revealed a link between inflammation and overactivation of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling in syndromes associated with aging. Pseudoxanthoma elasticum (PXE), a rare autosomal-recessive disorder, arises from mutations in ATP-binding cassette subfamily C member 6 (ABCC6). On a molecular level, PXE shares similarities with Hutchinson–Gilford progeria syndrome, such as increased activity of senescence-associated- beta-galactosidase or high expression of inflammatory factors. Thus, this study’s aim was the evaluation of activated STAT3 and the influence of JAK1/2-inhibitor baricitinib (BA) on inflammatory processes such as the complement system in PXE. Analysis of activation of STAT3 was performed by immunofluorescence and Western blot, while inflammatory processes and complement system factors were determined based on mRNA expression and protein level. Our results assume overactivation of JAK/STAT3 signaling, increased expression levels of several complement factors and high C3 protein concentration in the sera of PXE patients. Supplementation with BA reduces JAK/STAT3 activation and partly reduces inflammation as well as the gene expression of complement factors belonging to the C1 complex and C3 convertase in PXE fibroblasts. Our results indicate a link between JAK/STAT3 signaling and complement activation contributing to the proinflammatory phenotype in PXE fibroblasts. Full article
(This article belongs to the Special Issue Inflammation and Immunosenescence in Age-Related Diseases)
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Review

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11 pages, 796 KiB  
Review
Legend or Truth: Mature CD4+CD8+ Double-Positive T Cells in the Periphery in Health and Disease
by Magdalena Hagen, Luca Pangrazzi, Lourdes Rocamora-Reverte and Birgit Weinberger
Biomedicines 2023, 11(10), 2702; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11102702 - 05 Oct 2023
Cited by 2 | Viewed by 2737
Abstract
The expression of CD4 and CD8 co-receptors defines two distinct T cell populations with specialized functions. While CD4+ T cells support and modulate immune responses through different T-helper (Th) and regulatory subtypes, CD8+ T cells eliminate cells that might threaten the [...] Read more.
The expression of CD4 and CD8 co-receptors defines two distinct T cell populations with specialized functions. While CD4+ T cells support and modulate immune responses through different T-helper (Th) and regulatory subtypes, CD8+ T cells eliminate cells that might threaten the organism, for example, virus-infected or tumor cells. However, a paradoxical population of CD4+CD8+ double-positive (DP) T cells challenging this paradigm has been found in the peripheral blood. This subset has been observed in healthy as well as pathological conditions, suggesting unique and well-defined functions. Furthermore, DP T cells express activation markers and exhibit memory-like features, displaying an effector memory (EM) and central memory (CM) phenotype. A subset expressing high CD4 (CD4bright+) and intermediate CD8 (CD8dim+) levels and a population of CD8bright+CD4dim+ T cells have been identified within DP T cells, suggesting that this small subpopulation may be heterogeneous. This review summarizes the current literature on DP T cells in humans in health and diseases. In addition, we point out that strategies to better characterize this minor T cell subset’s role in regulating immune responses are necessary. Full article
(This article belongs to the Special Issue Inflammation and Immunosenescence in Age-Related Diseases)
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Other

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12 pages, 3252 KiB  
Brief Report
Senescence-Driven Inflammatory and Trophic Microenvironment Imprints Mesenchymal Stromal/Stem Cells in Osteoarthritic Patients
by Giuseppe Fusi, Michael Constantinides, Christina Fissoun, Lydiane Pichard, Yves-Marie Pers, Rosanna Ferreira-Lopez, Veronique Pantesco, Christophe Poulet, Olivier Malaise, Dominique De Seny, Jean-Marc Lemaitre, Christian Jorgensen and Jean-Marc Brondello
Biomedicines 2023, 11(7), 1994; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11071994 - 14 Jul 2023
Viewed by 1087
Abstract
Senescent cells promote progressive tissue degeneration through the establishment of a combined inflammatory and trophic microenvironment. The cellular senescence state has therefore emerged as a central driving mechanism of numerous age-related diseases, including osteoarthritis (OA), the most common rheumatic disease. Senescence hallmarks are [...] Read more.
Senescent cells promote progressive tissue degeneration through the establishment of a combined inflammatory and trophic microenvironment. The cellular senescence state has therefore emerged as a central driving mechanism of numerous age-related diseases, including osteoarthritis (OA), the most common rheumatic disease. Senescence hallmarks are detectable in chondrocytes, synoviocytes and sub-chondral bone cells. This study investigates how the senescence-driven microenvironment could impact the cell fate of resident osteoarticular mesenchymal stromal/stem cells (MSCs) that are hence contributing to OA disease progression. For that purpose, we performed a comparative gene expression analysis of MSCs isolated from healthy donors that were in vitro chronically exposed either to interferon-gamma (IFN-γ) or Transforming Growth Factor beta 1 (TGFβ1), two archetypical factors produced by senescent cells. Both treatments reduced MSC self-renewal capacities by upregulating different senescence-driven cycle-dependent kinase inhibitors. Furthermore, a common set of differentially expressed genes was identified in both treated MSCs that was also found enriched in MSCs isolated from OA patients. These findings highlight an imprinting of OA MSCs by the senescent joint microenvironment that changes their matrisome gene expression. Altogether, this research gives new insights into OA etiology and points to new innovative therapeutic opportunities to treat OA patients. Full article
(This article belongs to the Special Issue Inflammation and Immunosenescence in Age-Related Diseases)
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