Immunity & Ageing最新文献

{"title":"Correction: The impact of ageing on the distribution of preformed anti-HLA and anti-MICA antibody specificities in recipients from eastern China prior to initial HSCT","authors":"Qinqin Pan, Xiao Ma, Yajie You, Yuejiao Yu, Su Fan, Xiaoyan Wang, Mengyuan Wang, Ming Gao, Guangming Gong, Kourong Miao, Jie Shen, Xiaoyu Zhou","doi":"10.1186/s12979-024-00428-1","DOIUrl":"https://doi.org/10.1186/s12979-024-00428-1","url":null,"abstract":"<p><b>Correction: Immun Ageing 21, 15 (2024)</b>.</p><p><b>https://doi.org/10.1186/s12979-024-00417-4</b></p><p>Following publication of the original article [1], the Editors-in-Chief of <i>Immunity &amp; Ageing</i> requested to update the article title with the approval of the authors from “Ageing on the impact of distribution about preformed anti‑HLA and anti‑MICA antibody specificities in recipients prior to initial HSCT from East China” to “The impact of ageing on the distribution of preformed anti-HLA and anti-MICA antibody specificities in recipients from eastern China prior to initial HSCT’.</p><p>The original article [1] has been updated.</p><ol data-track-component=\"outbound reference\"><li data-counter=\"1.\"><p>Pan Q, Ma X, You Y et al. The impact of ageing on the distribution of preformed anti-HLA and anti-MICA antibody specificities in recipients from eastern China prior to initial HSCT. Immun Ageing 21, 15 (2024). https://doi.org/10.1186/s12979-024-00417-4.</p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>HLA Lab, Department of Transfusion, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, 210029, China</p><p>Qinqin Pan, Xiao Ma, Yajie You, Yuejiao Yu, Su Fan, Xiaoyan Wang, Mengyuan Wang, Jie Shen &amp; Xiaoyu Zhou</p></li><li><p>Department of Pharmacy, Jinling Hospital, Nanjing University School of Medicine, Nanjing, 210002, China</p><p>Ming Gao &amp; Guangming Gong</p></li><li><p>Department of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, 210029, China</p><p>Kourong Miao</p></li></ol><span>Authors</span><ol><li><span>Qinqin Pan</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Xiao Ma</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yajie You</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yuejiao Yu</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Su Fan</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Xiaoyan Wang</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Mengyuan Wang</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Ming Gao</span>View author publications<p>You can also search for this author in <s","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140567110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of germinal center and CD39highCD73+ B cells in the age-related tonsillar involution","authors":"Rocío Pastor, Juliana Puyssegur, M. Paula de la Guardia, Lindybeth Sarmiento Varón, Gladys Beccaglia, Nicolás Spada, Andrea Paes de Lima, M. Soledad Collado, Andrés Blanco, Isabel Aspe Scetti, M. Elena Arabolaza, Bibiana Paoli, Fernando Chirdo, Eloísa Arana","doi":"10.1186/s12979-024-00425-4","DOIUrl":"https://doi.org/10.1186/s12979-024-00425-4","url":null,"abstract":"The tonsils operate as a protection ring of mucosa at the gates of the upper aero-digestive tract. They show similarities with lymph nodes and participate as inductive organs of systemic and mucosal immunity. Based on the reduction of their size since puberty, they are thought to experience involution in adulthood. In this context, we have used tonsillar mononuclear cells (TMC) isolated from patients at different stages of life, to study the effect of ageing and the concomitant persistent inflammation on these immune cells. We found an age-dependent reduction in the proportion of germinal center B cell population (BGC) and its T cell counterpart (T follicular helper germinal center cells, TfhGC). Also, we demonstrated an increment in the percentage of local memory B cells and mantle zone T follicular helper cells (mTfh). Furthermore, younger tonsils rendered higher proportion of proliferative immune cells within the freshly isolated TMC fraction than those from older ones. We demonstrated the accumulation of a B cell subset (CD20+CD39highCD73+ cells) metabolically adapted to catabolize adenosine triphosphate (ATP) as patients get older. To finish, tonsillar B cells from patients at different ages did not show differences in their proliferative response to stimulation ex vivo, in bulk TMC cultures. This paper sheds light on the changing aspects of the immune cellular landscape, over the course of time and constant exposure, at the entrance of the respiratory and digestive systems. Our findings support the notion that there is a re-modelling of the immune functionality of the excised tonsils over time. They are indicative of a transition from an effector type of immune response, typically oriented to reduce pathogen burden early in life, to the development of an immunosuppressive microenvironment at later stages, when tissue damage control gets critical provided the time passed under immune attack. Noteworthy, when isolated from such histologic microenvironment, older tonsillar B cells seem to level their proliferation capacity with the younger ones. Understanding these features will not only contribute to comprehend the differences in susceptibility to pathogens among children and adults but would also impact on vaccine developments intended to target these relevant mucosal sites.","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140566815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Addition of inflammation-related biomarkers to the CAIDE model for risk prediction of all-cause dementia, Alzheimer’s disease and vascular dementia in a prospective study","authors":"Kira Trares, Manuel Wiesenfarth, Hannah Stocker, Laura Perna, Agnese Petrera, Stefanie M. Hauck, Konrad Beyreuther, Hermann Brenner, Ben Schöttker","doi":"10.1186/s12979-024-00427-2","DOIUrl":"https://doi.org/10.1186/s12979-024-00427-2","url":null,"abstract":"It is of interest whether inflammatory biomarkers can improve dementia prediction models, such as the widely used Cardiovascular Risk Factors, Aging and Dementia (CAIDE) model. The Olink Target 96 Inflammation panel was assessed in a nested case-cohort design within a large, population-based German cohort study (n = 9940; age-range: 50–75 years). All study participants who developed dementia over 20 years of follow-up and had complete CAIDE variable data (n = 562, including 173 Alzheimer’s disease (AD) and 199 vascular dementia (VD) cases) as well as n = 1,356 controls were selected for measurements. 69 inflammation-related biomarkers were eligible for use. LASSO logistic regression and bootstrapping were utilized to select relevant biomarkers and determine areas under the curve (AUCs). The CAIDE model 2 (including Apolipoprotein E (APOE) ε4 carrier status) predicted all-cause dementia, AD, and VD better than CAIDE model 1 (without APOE ε4) with AUCs of 0.725, 0.752 and 0.707, respectively. Although 20, 7, and 4 inflammation-related biomarkers were selected by LASSO regression to improve CAIDE model 2, the AUCs did not increase markedly. CAIDE models 1 and 2 generally performed better in mid-life (50–64 years) than in late-life (65–75 years) sub-samples of our cohort, but again, inflammation-related biomarkers did not improve their predictive abilities. Despite a lack of improvement in dementia risk prediction, the selected inflammation-related biomarkers were significantly associated with dementia outcomes and may serve as a starting point to further elucidate the pathogenesis of dementia.","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140566814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"B-1 derived anti-Thy-1 B cells in old aged mice develop lymphoma/leukemia with high expression of CD11b and Hamp2 that different from TCL1 transgenic mice","authors":"Kyoko Hayakawa, Yan Zhou, Susan A. Shinton","doi":"10.1186/s12979-024-00415-6","DOIUrl":"https://doi.org/10.1186/s12979-024-00415-6","url":null,"abstract":"Human old aged unmutated chronic lymphocytic leukemia U-CLL are the TCL1+ZAP70+CD5+ B cells. Since CD5 makes the BCR signaling tolerance, ZAP70 increased in U-CLL not only TCL1+ alone. In mice, TCL1 (TCL1A) is the negative from neonate to old aged, as TC–. VH8-12/Vk21-5 is the anti-thymocyte/Thy-1 autoreactive ATA B cell. When ATA μκTg generation in mice, ATA B cells are the neonate generated CD5+ B cells in B-1, and in the middle age, CD5+ can be down or continuously CD5+, then, old aged CLL/lymphoma generation with increased CD11b in TC–ZAP70–CD5– or TC–ZAP70+CD5+. In this old aged TC–ATA B microarray analysis showed most similar to human CLL and U-CLL, and TC–ZAP70+CD5+ showed certain higher present as U-CLL. Original neonate ATA B cells showed with several genes down or further increase in old aged tumor, and old aged T-bet+CD11c+, CTNNB1hi, HMGBhi, CXCR4hi, DPP4hi and decreased miR181b. These old aged increased genes and down miR181b are similar to human CLL. Also, in old age ATA B cell tumor, high CD38++CD44++, increased Ki67+ AID+, and decreased CD180– miR15Olow are similar to U-CLL. In this old aged ATA B, increased TLR7,9 and Wnt10b. TC+Tg generated with ATAμκTg mice occurred middle age tumor as TC+ZAP70–CD5+ or TC+ZAP70+CD5+, with high NF-kB1, TLR4,6 and Wnt5b,6 without increased CD11b. Since neonatal state to age with TC+Tg continuously, middle age CLL/lymphoma generation is not similar to old aged generated, however, some increased in TC+ZAP70+ are similar to the old age TC– ATA B tumor. Then, TC– ATA B old age tumor showed some difference to human CLL. ATA B cells showed CD11b+CD22++, CD24 down, and hepcidin Hamp2++ with iron down. This mouse V8-12 similar to human V2-5, and V2-5 showed several cancers with macrophages/neutrophils generated hepcidin+ ironlow or some showed hepcidin– iron+ with tumor, and mouse V8-12 with different Vk19-17 generate MZ B cells strongly increased macrophage++ in old aged and generated intestine/colon tumor. Conclusion, neonate generated TC–ATA B1 cells in old aged tumor generation are CD11b+ in the leukemia CLL together with lymphoma cancer with hepcidin-related Hamp2++ in B-1 cell generation to control iron.","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140567112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in the innate immune response to SARS-CoV-2 with advancing age in humans.","authors":"Sudhanshu Agrawal, Michelle Thu Tran, Tara Sinta Kartika Jennings, Marlaine Maged Hosny Soliman, Sally Heo, Bobby Sasson, Farah Rahmatpanah, Anshu Agrawal","doi":"10.1186/s12979-024-00426-3","DOIUrl":"10.1186/s12979-024-00426-3","url":null,"abstract":"<p><strong>Background: </strong>Advancing age is a major risk factor for respiratory viral infections. The infections are often prolonged and difficult to resolve resulting hospitalizations and mortality. The recent COVID-19 pandemic has highlighted this as elderly subjects have emerged as vulnerable populations that display increased susceptibility and severity to SARS-CoV-2. There is an urgent need to identify the probable mechanisms underlying this to protect against future outbreaks of such nature. Innate immunity is the first line of defense against viruses and its decline impacts downstream immune responses. This is because dendritic cells (DCs) and macrophages are key cellular elements of the innate immune system that can sense and respond to viruses by producing inflammatory mediators and priming CD4 and CD8 T-cell responses.</p><p><strong>Results: </strong>We investigated the changes in innate immune responses to SARS-CoV-2 as a function of age. Our results using human PBMCs from aged, middle-aged, and young subjects indicate that the activation of DCs and monocytes in response to SARS-CoV-2 is compromised with age. The impairment is most apparent in pDCs where both aged and middle-aged display reduced responses. The secretion of IL-29 that confers protection against respiratory viruses is also decreased in both aged and middle-aged subjects. In contrast, inflammatory mediators associated with severe COVID-19 including CXCL-8, TREM-1 are increased with age. This is also apparent in the gene expression data where pathways related host defense display an age dependent decrease with a concomitant increase in inflammatory pathways. Not only are the inflammatory pathways and mediators increased after stimulation with SARS-CoV-2 but also at homeostasis. In keeping with reduced DC activation, the induction of cytotoxic CD8 T cells is also impaired in aged subjects. However, the CD8 T cells from aged subjects display increased baseline activation in accordance with the enhanced baseline inflammation.</p><p><strong>Conclusions: </strong>Our results demonstrate a decline in protective anti-viral immune responses and increase in damaging inflammatory responses with age indicating that dysregulated innate immune responses play a significant role in the increased susceptibility of aged subjects to COVID-19. Furthermore, the dysregulation in immune responses develops early on as middle-aged demonstrate several of these changes.</p>","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10956333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140186347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune profiles of pre-frail people living with HIV-1: a prospective longitudinal study.","authors":"Lucy Kundura, Renaud Cezar, Sandrine Gimenez, Manuela Pastore, Christelle Reynes, Albert Sotto, Jacques Reynes, Clotilde Allavena, Laurence Meyer, Alain Makinson, Pierre Corbeau","doi":"10.1186/s12979-024-00416-5","DOIUrl":"10.1186/s12979-024-00416-5","url":null,"abstract":"<p><strong>Background: </strong>People living with HIV (PLWH) are at risk of frailty, which is predictive for death. As an overactivity of the immune system is thought to fuel frailty, we characterized the immune activation profiles linked to frailty.</p><p><strong>Methods: </strong>We quantified twenty-seven activation markers in forty-six virological responders (four females and forty-two males; median age, 74 years; median duration of infection, 24 years; median duration of undetectability, 13 years), whose frailty was determined according to the Fried criteria. T cell and NK cell activation was evaluated by flow cytometry, using a panel of cell surface markers. Soluble markers of inflammation, and monocyte activation and endothelial activation were measured by ELISA. The participants' immune activation was profiled by an unsupervised double hierarchical clustering analysis. We used ANOVA p-values to rank immunomarkers most related to Fried score. A Linear Discriminant Analysis (LDA) was performed to link immune activation markers to frailty.</p><p><strong>Results: </strong>41% of the participants were pre-frail, including 24% with a Fried score of 1, and 17% with a Fried score of 2. ANOVA identified the 14 markers of T cell, monocyte, NK cell, endothelial activation, and inflammation the most linked to Fried 3 classes. The LDA performed with these 14 markers was capable of discriminating volunteers according to their Fried score. Two out of the 5 immune activation profiles revealed by the hierarchical clustering were linked to and predictive of pre-frailty. These two profiles were characterized by a low percentage of CD4 T cells and a high percentage of CD8 T cells, activated CD4 T cells, CD8 T cells, and NK cells, and inflammation.</p><p><strong>Conclusions: </strong>We identified a particular immune activation profile associated with pre-frailty in PLWH. Profiling participants at risk of developing frailty might help to tailor the screening and prevention of medical complications fueled by loss of robustness. Further studies will indicate whether this frailty signature is specific or not of HIV infection, and whether it also precedes frailty in the general population.</p>","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10935995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140121354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longevity-associated BPIFB4 gene counteracts the inflammatory signaling.","authors":"Monica Cattaneo, Andrea Baragetti, Alberto Malovini, Elena Ciaglia, Valentina Lopardo, Elena Olmastroni, Manuela Casula, Carolina Ciacci, Alberico L Catapano, Annibale A Puca","doi":"10.1186/s12979-024-00424-5","DOIUrl":"10.1186/s12979-024-00424-5","url":null,"abstract":"<p><strong>Background: </strong>Increased levels of pro-inflammatory proteins in plasma can be detected in older individuals and associate with the so called chronic low-grade inflammation, which contributes to a faster progression of aged-related cardiovascular (CV) diseases, including frailty, neurodegeneration, gastro-intestinal diseases and disorders reflected by alterations in the composition of gut microbiota. However, successful genetic programme of long-living individuals alters the trajectory of the ageing process, by promoting an efficient immune response that can counterbalance deleterious effects of inflammation and the CV complications. This is the case of BPIFB4 gene in which, homozygosity for a four single-nucleotide polymorphism (SNP) haplotype, the Longevity-Associated Variant (LAV) correlates with prolonged health span and reduced risk of CV complications and inflammation. The relation between LAV-BPIFB4 and inflammation has been proven in different experimental models, here we hypothesized that also human homozygous carriers of LAV-BPIFB4 gene may experience a lower inflammatory burden as detected by plasma proteomics that could explain their favourable CV risk trajectory over time. Moreover, we explored the therapeutic effects of LAV-BPIFB4 in inflammatory disease and monolayer model of intestinal barrier.</p><p><strong>Results: </strong>We used high-throughput proteomic approach to explore the profiles of circulating proteins from 591 baseline participants selected from the PLIC cohort according to the BPIFB4 genotype to identify the signatures and differences of BPIFB4 genotypes useful for health and disease management. The observational analysis identified a panel of differentially expressed circulating proteins between the homozygous LAV-BPIFB4 carriers and the other alternative BPIFB4 genotypes highlighting in the latter ones a higher grade of immune-inflammatory markers. Moreover, in vitro studies performed on intestinal epithelial organs from inflammatory bowel disease (IBD) patients and monolayer model of intestinal barrier demonstrated the benefit of LAV-BPIFB4 treatment.</p><p><strong>Conclusions: </strong>Homozygosity for LAV-BPIFB4 results in the attenuation of inflammation in PLIC cohort and IBD patients providing preliminary evidences for its therapeutic use in inflammatory disorders that need to be further characterized and confirmed by independent studies.</p>","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10929107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140102809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Excess of body weight is associated with accelerated T-cell senescence in hospitalized COVID-19 patients.","authors":"Mailton Prestes Madruga, Lucas Kich Grun, Letícya Simone Melo Dos Santos, Frederico Orlando Friedrich, Douglas Bitencourt Antunes, Marcella Elesbão Fogaça Rocha, Pedro Luis Silva, Gilson P Dorneles, Paula Coelho Teixeira, Tiago Franco Oliveira, Pedro R T Romão, Lucas Santos, José Claudio Fonseca Moreira, Vinicius Schenk Michaelsen, Marcelo Cypel, Marcos Otávio Brum Antunes, Marcus Herbert Jones, Florencia María Barbé-Tuana, Moisés Evandro Bauer","doi":"10.1186/s12979-024-00423-6","DOIUrl":"10.1186/s12979-024-00423-6","url":null,"abstract":"<p><strong>Background: </strong>Several risk factors have been involved in the poor clinical progression of coronavirus disease-19 (COVID-19), including ageing, and obesity. SARS-CoV-2 may compromise lung function through cell damage and paracrine inflammation; and obesity has been associated with premature immunosenescence, microbial translocation, and dysfunctional innate immune responses leading to poor immune response against a range of viruses and bacterial infections. Here, we have comprehensively characterized the immunosenescence, microbial translocation, and immune dysregulation established in hospitalized COVID-19 patients with different degrees of body weight.</p><p><strong>Results: </strong>Hospitalised COVID-19 patients with overweight and obesity had similarly higher plasma LPS and sCD14 levels than controls (all p < 0.01). Patients with obesity had higher leptin levels than controls. Obesity and overweight patients had similarly higher expansions of classical monocytes and immature natural killer (NK) cells (CD56⁺CD16^-) than controls. In contrast, reduced proportions of intermediate monocytes, mature NK cells (CD56⁺CD16⁺), and NKT were found in both groups of patients than controls. As expected, COVID-19 patients had a robust expansion of plasmablasts, contrasting to lower proportions of major T-cell subsets (CD4 + and CD8+) than controls. Concerning T-cell activation, overweight and obese patients had lower proportions of CD4⁺CD38⁺ cells than controls. Contrasting changes were reported in CD25⁺CD127^low/neg regulatory T cells, with increased and decreased proportions found in CD4⁺ and CD8⁺ T cells, respectively. There were similar proportions of T cells expressing checkpoint inhibitors across all groups. We also investigated distinct stages of T-cell differentiation (early, intermediate, and late-differentiated - TEMRA). The intermediate-differentiated CD4 + T cells and TEMRA cells (CD4⁺ and CD8⁺) were expanded in patients compared to controls. Senescent T cells can also express NK receptors (NKG2A/D), and patients had a robust expansion of CD8⁺CD57⁺NKG2A⁺ cells than controls. Unbiased immune profiling further confirmed the expansions of senescent T cells in COVID-19.</p><p><strong>Conclusions: </strong>These findings suggest that dysregulated immune cells, microbial translocation, and T-cell senescence may partially explain the increased vulnerability to COVID-19 in subjects with excess of body weight.</p>","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10921685/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140061205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune aging in annual killifish.","authors":"Gabriele Morabito, Alina Ryabova, Dario Riccardo Valenzano","doi":"10.1186/s12979-024-00418-3","DOIUrl":"10.1186/s12979-024-00418-3","url":null,"abstract":"<p><p>Turquoise killifish (Nothobranchius furzeri) evolved a naturally short lifespan of about six months and exhibit aging hallmarks that affect multiple organs. These hallmarks include protein aggregation, telomere shortening, cellular senescence, and systemic inflammation. Turquoise killifish possess the full spectrum of vertebrate-specific innate and adaptive immune system. However, during their recent evolutionary history, they lost subsets of mucosal-specific antibody isoforms that are present in other teleosts. As they age, the immune system of turquoise killifish undergoes dramatic cellular and systemic changes. These changes involve increased inflammation, reduced antibody diversity, an increased prevalence of pathogenic microbes in the intestine, and extensive DNA damage in immune progenitor cell clusters. Collectively, the wide array of age-related changes occurring in turquoise killifish suggest that, despite an evolutionary separation spanning hundreds of millions of years, teleosts and mammals share common features of immune system aging. Hence, the spontaneous aging observed in the killifish immune system offers an excellent opportunity for discovering fundamental and conserved aspects associated with immune system aging across vertebrates. Additionally, the species' naturally short lifespan of only a few months, along with its experimental accessibility, offers a robust platform for testing interventions to improve age-related dysfunctions in the whole organism and potentially inform the development of immune-based therapies for human aging-related diseases.</p>","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10921792/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140066201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Obesity-induced neuroinflammation and cognitive impairment in young adult versus middle-aged mice","authors":"Rosemary E. Henn, Sarah E. Elzinga, Emily Glass, Rachel Parent, Kai Guo, Adam M. Allouch, Faye E. Mendelson, John Hayes, Ian Webber-Davis, Geoffery G. Murphy, Junguk Hur, Eva L. Feldman","doi":"10.1186/s12979-024-00422-7","DOIUrl":"https://doi.org/10.1186/s12979-024-00422-7","url":null,"abstract":"<p><b>Correction: Immun Ageing 19, 67 (2022)</b></p><p><b>https://doi.org/10.1186/s12979-022-00323-7</b></p><p>Following publication of the original article [1], the authors identified an error in the author name of Adam M. Allouch.</p><p>The incorrect author name is: Adam A. Allouch.</p><p>The correct author name is: Adam M. Allouch.</p><p>The author group has been updated above and the original article [1] has been corrected.</p><ol data-track-component=\"outbound reference\"><li data-counter=\"1.\"><p>Henn RE, Elzinga SE, Glass E, et al. Obesity-induced neuroinflammation and cognitive impairment in young adult versus middle-aged mice. Immun Ageing. 2022;19:67. https://doi.org/10.1186/s12979-022-00323-7.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><span>Author notes</span><ol><li><p>Rosemary E. Henn and Sarah E. Elzinga contributed equally to this work.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>Department of Neurology, University of Michigan, Ann Arbor, MI, 48109, USA</p><p>Rosemary E. Henn, Sarah E. Elzinga, Adam M. Allouch, Faye E. Mendelson, John Hayes, Ian Webber-Davis &amp; Eva L. Feldman</p></li><li><p>NeuroNetwork for Emerging Therapies, University of Michigan, Ann Arbor, MI, 48109, USA</p><p>Rosemary E. Henn, Sarah E. Elzinga, Adam M. Allouch, Faye E. Mendelson, John Hayes, Ian Webber-Davis &amp; Eva L. Feldman</p></li><li><p>Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI, 48109, USA</p><p>Emily Glass, Rachel Parent &amp; Geoffery G. Murphy</p></li><li><p>Department of Molecular and Integrative Physiology, Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, MI, 48109, USA</p><p>Emily Glass, Rachel Parent &amp; Geoffery G. Murphy</p></li><li><p>Department of Biomedical Sciences, University of North Dakota, Grand Forks, ND, 58202, USA</p><p>Kai Guo &amp; Junguk Hur</p></li></ol><span>Authors</span><ol><li><span>Rosemary E. Henn</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Sarah E. Elzinga</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Emily Glass</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Rachel Parent</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Kai Guo</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Adam M. Allouch</span>View author publications<p>You can also search for this author in <span>PubMed<span> <","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139918698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}