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Cells
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Inflammaging: The Immunology of Aging—Series 2
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Inflammaging: The Immunology of Aging—Series 2

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

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 2043

Special Issue Editor

Dr. Juan Pablo de Rivero Vaccari

E-Mail Website
Guest Editor
1. Department of Neurological Surgery and The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL 33136, USA
2. Neuroscience Graduate Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA
3. Cellular Physiology and Molecular Biophysics Graduate Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA
4. Center for Cognitive Neuroscience and Aging, University of Miami Miller School of Medicine, Miami, FL 33136, USA
Interests: inflammasome; neuroinflammation; traumatic brain injury; spinal cord injury; stroke; Alzheimer’s disease; Parkinson’s disease; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is my pleasure to invite you to contribute to the second edition of Inflammaging: The Immunology of Aging that previously published 15 papers.

Several factors contribute to the aging process. These factors include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication. Together, these are referred to as “the Hallmarks of Aging”. A characteristic feature of altered intercellular communication is inflammaging or age-related inflammation. Dysregulation of the innate and/or adaptive immune response contributes to inflammaging, which is believed to be a predecessor to the development of age-related diseases such as Alzheimer’s disease, Parkinson’s disease, age-related macular degeneration, obesity, type 2 diabetes and atherosclerosis, among others.

We invite all scientists working on the immunology of age-related conditions or diseases to participate in this Special Issue. Original research articles, reviews on all aspects related to the immunology of aging and age-related processes are welcome. Articles with insights from a cell and molecular biological perspective are especially welcome. Relevant topics include, but are not limited to: inflammaging and oxidative stress, age-related cardiovascular diseases, role of extracellular vesicle biology in inflammaging, inflammasome regulation in aging and age-related diseases, inflammation and neurodegeneration, inflammation and joint degeneration, inflammaging and the gut microbiome, and inflammaging and cancer, among others.

Dr. Juan Pablo de Rivero Vaccari
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. 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

  • inflammaging
  • innate immunity
  • adaptive immunity
  • inflammasomes
  • aging
  • Alzheimer’s disease
  • Parkinson’s disease
  • stroke
  • extracellular vesicles
  • macular degeneration
  • obesity
  • diabetes
  • atherosclerosis
  • biomarkers

Related Special Issue

Published Papers (2 papers)

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Research

14 pages, 2267 KiB  
Article
Immunity in the Progeroid Model of Cockayne Syndrome: Biomarkers of Pathological Aging
by Khouloud Zayoud, Asma Chikhaoui, Ichraf Kraoua, Anis Tebourbi, Dorra Najjar, Saker Ayari, Ines Safra, Imen Kraiem, Ilhem Turki, Samia Menif and Houda Yacoub-Youssef
Cells 2024, 13(5), 402; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13050402 - 26 Feb 2024
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Abstract
Cockayne syndrome (CS) is a rare autosomal recessive disorder that affects the DNA repair process. It is a progeroid syndrome predisposing patients to accelerated aging and to increased susceptibility to respiratory infections. Here, we studied the immune status of CS patients to determine [...] Read more.
Cockayne syndrome (CS) is a rare autosomal recessive disorder that affects the DNA repair process. It is a progeroid syndrome predisposing patients to accelerated aging and to increased susceptibility to respiratory infections. Here, we studied the immune status of CS patients to determine potential biomarkers associated with pathological aging. CS patients, as well as elderly and young, healthy donors, were enrolled in this study. Complete blood counts for patients and donors were assessed, immune cell subsets were analyzed using flow cytometry, and candidate cytokines were analyzed via multi-analyte ELISArray kits. In CS patients, we noticed a high percentage of lymphocytes, an increased rate of intermediate and non-classical monocytes, and a high level of pro-inflammatory cytokine IL-8. In addition, we identified an increased rate of particular subtypes of T Lymphocyte CD8+ CD28− CD27−, which are senescent T cells. Thus, an inflammatory state was found in CS patients that is similar to that observed in the elderly donors and is associated with an immunosenescence status in both groups. This could explain the CS patients’ increased susceptibility to infections, which is partly due to an aging-associated inflammation process. Full article
(This article belongs to the Special Issue Inflammaging: The Immunology of Aging—Series 2)
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14 pages, 1967 KiB  
Article
The Relationship between p-tau217, p-tau231, and p-tau205 in the Human Brain Is Affected by the Cellular Environment and Alzheimer’s Disease Pathology
by Malin Wennström, Nina Schultz, Paula Mille Gallardo, The Netherlands Brain Bank, Geidy E. Serrano, Thomas G. Beach, Suchira Bose and Oskar Hansson
Cells 2024, 13(4), 331; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13040331 - 11 Feb 2024
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Abstract
The levels of p-tau217 and p-tau231 in cerebrospinal fluid (CSF) are associated with early amyloid beta (Aß) changes in the brain, while the CSF levels of p-tau205 are foremost related to tau pathology in the later stages of the disease. To investigate if [...] Read more.
The levels of p-tau217 and p-tau231 in cerebrospinal fluid (CSF) are associated with early amyloid beta (Aß) changes in the brain, while the CSF levels of p-tau205 are foremost related to tau pathology in the later stages of the disease. To investigate if the three p-tau variants are found to the same degree in different tau structures and if their co-localization is affected by the diagnosis and presence of Aß plaques, we immunostained sections of the entorhinal cortex (EC) and inferior temporal gyrus (ITG) from non-demented controls (NC), patients with Alzheimer’s disease (AD), and primary age-related tauopathy (PART) against p-tau217, p-tau231, and p-tau205 together with Methoxi-X04. An analysis using confocal microscopy showed that the co-localization variable, the Pearson correlation coefficient (PCC), was significantly higher between p-tau231 and p-tau205 in neurofibrillary tangles compared to neuropil threads and dystrophic neurites in plaques. The PCC value between all three p-tau variants in the neuropil threads was significantly lower in the ECs of patients with AD compared to the NC and in the ITGs of patients with AD, with a high Aß load compared to PART. The lowered value was associated with proportionally higher amounts of non-colocalized p-tau231 and p-tau217 compared to p-tau205, and the PCC values were negatively correlated with Aß and the tangle loads in patients with AD, but positively correlated with tangles in PART. These results suggest that the proportion of and co-localization between p-tau217, p-tau231, and p-tau205 are dependent on cellular localization and are altered in response to AD pathology in a spatial–temporal manner. Full article
(This article belongs to the Special Issue Inflammaging: The Immunology of Aging—Series 2)
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