Seminars in Immunopathology最新文献

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Causes and costs of global COVID-19 vaccine inequity. 全球新冠肺炎疫苗不公平的原因和代价。
IF 9 2区 医学
Seminars in Immunopathology Pub Date : 2024-01-01 Epub Date: 2023-10-23 DOI: 10.1007/s00281-023-00998-0
Maddalena Ferranna
{"title":"Causes and costs of global COVID-19 vaccine inequity.","authors":"Maddalena Ferranna","doi":"10.1007/s00281-023-00998-0","DOIUrl":"10.1007/s00281-023-00998-0","url":null,"abstract":"<p><p>Despite the rapid development of safe and effective COVID-19 vaccines and the widely recognized health and economic benefits of vaccination, there exist stark differences in vaccination rates across country income groups. While more than 70% of the population is fully vaccinated in high-income countries, vaccination rates in low-income countries are only around 30%. The paper reviews the factors behind global COVID-19 vaccine inequity and the health, social, and economic costs triggered by this inequity. The main contributors to vaccine inequity include vaccine nationalism, intellectual property rights, constraints in manufacturing capacity, poor resilience of healthcare systems, and vaccine hesitancy. Vaccine inequity has high costs, including preventable deaths and cases of illnesses in low-income countries, slow economic recovery, and large learning losses among children. Increasing vaccination rates in low-income countries is in the self-interest of higher-income countries as it may prevent the emergence of new variants and continuous disruptions to global supply chains.</p>","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":" ","pages":"469-480"},"PeriodicalIF":9.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11136847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49692282","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}
引用次数: 0
Physiological and immunological barriers in the lung. 肺部的生理和免疫屏障。
IF 9 2区 医学
Seminars in Immunopathology Pub Date : 2024-01-01 Epub Date: 2024-03-07 DOI: 10.1007/s00281-024-01003-y
Takahiro Kageyama, Takashi Ito, Shigeru Tanaka, Hiroshi Nakajima
{"title":"Physiological and immunological barriers in the lung.","authors":"Takahiro Kageyama, Takashi Ito, Shigeru Tanaka, Hiroshi Nakajima","doi":"10.1007/s00281-024-01003-y","DOIUrl":"10.1007/s00281-024-01003-y","url":null,"abstract":"<p><p>The lungs serve as the primary organ for respiration, facilitating the vital exchange of gases with the bloodstream. Given their perpetual exposure to external particulates and pathogens, they possess intricate protective barriers. Cellular adhesion in the lungs is robustly maintained through tight junctions, adherens junctions, and desmosomes. Furthermore, the pulmonary system features a mucociliary clearance mechanism that synthesizes mucus and transports it to the outside. This mucus is enriched with chemical barriers like antimicrobial proteins and immunoglobulin A (IgA). Additionally, a complex immunological network comprising epithelial cells, neural cells, and immune cells plays a pivotal role in pulmonary defense. A comprehensive understanding of these protective systems offers valuable insights into potential pathologies and their therapeutic interventions.</p>","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":" ","pages":"533-547"},"PeriodicalIF":9.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11136722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140050357","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}
引用次数: 0
Epithelial recognition and elimination against aberrant cells. 上皮细胞识别和消除异常细胞。
IF 9 2区 医学
Seminars in Immunopathology Pub Date : 2024-01-01 Epub Date: 2024-02-27 DOI: 10.1007/s00281-024-01001-0
Shiyu Ayukawa, Nagisa Kamoshita, Takeshi Maruyama
{"title":"Epithelial recognition and elimination against aberrant cells.","authors":"Shiyu Ayukawa, Nagisa Kamoshita, Takeshi Maruyama","doi":"10.1007/s00281-024-01001-0","DOIUrl":"10.1007/s00281-024-01001-0","url":null,"abstract":"<p><p>Epithelial cells, which are non-immune cells, not only function as a physical defence barrier but also continuously monitor and eliminate aberrant epithelial cells in their vicinity. In other words, it has become evident that epithelial cells possess immune cell-like functions. In fact, recent research has revealed that epithelial cells recognise the Major Histocompatibility Complex I (MHC-I) of aberrant cells as a mechanism for surveillance. This cellular defence mechanism of epithelial cells probably detects aberrant cells more promptly than the conventional immune response, making it a novel and primary biological defence. Furthermore, there is the potential for this new immune-like biological defence mechanism to establish innovative treatment for disease prevention, leading to increasing anticipation for its future medical applications. In this review, we aim to summarise the recognition and attack mechanisms of aberrant cells by epithelial cells in mammals, with a particular focus on the field of cancer. Additionally, we discuss the potential therapeutic applications of epithelial cell-based defence against cancer, including novel prophylactic treatment methods based on molecular mechanisms.</p>","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":" ","pages":"521-532"},"PeriodicalIF":9.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139973355","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}
引用次数: 0
The overlooked bacterial pandemic. 被忽视的细菌大流行
IF 9 2区 医学
Seminars in Immunopathology Pub Date : 2024-01-01 Epub Date: 2023-12-11 DOI: 10.1007/s00281-023-00997-1
Danilo Gomes Moriel, Diego Piccioli, Maria Michelina Raso, Mariagrazia Pizza
{"title":"The overlooked bacterial pandemic.","authors":"Danilo Gomes Moriel, Diego Piccioli, Maria Michelina Raso, Mariagrazia Pizza","doi":"10.1007/s00281-023-00997-1","DOIUrl":"10.1007/s00281-023-00997-1","url":null,"abstract":"<p><p>The COVID-19 pandemic had a significant economic and health impact worldwide. It also reinforced the misperception that only viruses can pose a threat to human existence, overlooking that bacteria (e.g., plague and cholera) have severely haunted and shaped the course of human civilization. While the world is preparing for the next viral pandemic, it is again overlooking a silent one: antimicrobial resistance (AMR). This review proposes to show the impact of bacterial infections on civilization to remind the pandemic potential. The work will also discuss a few examples of how bacteria can mutate risking global spread and devastating outcomes, the effect on the global burden, and the prophylactic and therapeutic measures. Indeed, AMR is dramatically increasing and if the trend is not reversed, it has the potential to quickly turn into the most important health problem worldwide.</p>","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":" ","pages":"481-491"},"PeriodicalIF":9.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11136754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138809361","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}
引用次数: 0
The role of vaccines in the COVID-19 pandemic: what have we learned? 疫苗在 COVID-19 大流行中的作用:我们学到了什么?
IF 9 2区 医学
Seminars in Immunopathology Pub Date : 2024-01-01 Epub Date: 2023-07-12 DOI: 10.1007/s00281-023-00996-2
Florian Krammer
{"title":"The role of vaccines in the COVID-19 pandemic: what have we learned?","authors":"Florian Krammer","doi":"10.1007/s00281-023-00996-2","DOIUrl":"10.1007/s00281-023-00996-2","url":null,"abstract":"<p><p>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged late in 2019 and caused the coronavirus disease 2019 (COVID-19) pandemic that has so far claimed approximately 20 million lives. Vaccines were developed quickly, became available in the end of 2020, and had a tremendous impact on protection from SARS-CoV-2 mortality but with emerging variants the impact on morbidity was diminished. Here I review what we learned from COVID-19 from a vaccinologist's perspective.</p>","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":" ","pages":"451-468"},"PeriodicalIF":9.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11136744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10147591","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}
引用次数: 0
Sex differences in the inflammatory response to stroke. 中风炎症反应的性别差异。
IF 9 2区 医学
Seminars in Immunopathology Pub Date : 2023-05-01 Epub Date: 2022-11-10 DOI: 10.1007/s00281-022-00969-x
Muhammad Bilal Tariq, Juneyoung Lee, Louise D McCullough
{"title":"Sex differences in the inflammatory response to stroke.","authors":"Muhammad Bilal Tariq, Juneyoung Lee, Louise D McCullough","doi":"10.1007/s00281-022-00969-x","DOIUrl":"10.1007/s00281-022-00969-x","url":null,"abstract":"<p><p>Ischemic stroke is a leading cause of morbidity and mortality and disproportionally affects women, in part due to their higher longevity. Older women have poorer outcomes after stroke with high rates of cognitive deficits, depression, and reduced quality of life. Post-stroke inflammatory responses are also sexually dimorphic and drive differences in infarct size and recovery. Factors that influence sex-specific immune responses can be both intrinsic and extrinsic. Differences in gonadal hormone exposure, sex chromosome compliment, and environmental/social factors can drive changes in transcriptional and metabolic profiles. In addition, how these variables interact, changes across the lifespan. After the onset of ischemic injury, necrosis and apoptosis occur, which activate microglia and other glial cells within the central nervous system, promoting the release of cytokines and chemokines and neuroinflammation. Cells involved in innate and adaptive immune responses also have dual functions after stroke as they can enhance inflammation acutely, but also contribute to suppression of the inflammatory cascade and later repair. In this review, we provide an overview of the current literature on sex-specific inflammatory responses to ischemic stroke. Understanding these differences is critical to identifying therapeutic options for both men and women.</p>","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"45 3","pages":"295-313"},"PeriodicalIF":9.0,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10924671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10064719","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}
引用次数: 0
Unveiling the immunopathology of stroke: a comprehensive view on brain-immune interaction. 揭示脑卒中的免疫病理:脑免疫相互作用的综合观点。
IF 9 2区 医学
Seminars in Immunopathology Pub Date : 2023-05-01 DOI: 10.1007/s00281-023-00995-3
Tim Magnus, Arthur Liesz
{"title":"Unveiling the immunopathology of stroke: a comprehensive view on brain-immune interaction.","authors":"Tim Magnus,&nbsp;Arthur Liesz","doi":"10.1007/s00281-023-00995-3","DOIUrl":"https://doi.org/10.1007/s00281-023-00995-3","url":null,"abstract":"","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"45 3","pages":"279-280"},"PeriodicalIF":9.0,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10279564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10065766","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}
引用次数: 0
Role of alarmins in poststroke inflammation and neuronal repair. 警报器在脑卒中后炎症和神经元修复中的作用。
IF 9 2区 医学
Seminars in Immunopathology Pub Date : 2023-05-01 DOI: 10.1007/s00281-022-00961-5
Seiichiro Sakai, Takashi Shichita
{"title":"Role of alarmins in poststroke inflammation and neuronal repair.","authors":"Seiichiro Sakai,&nbsp;Takashi Shichita","doi":"10.1007/s00281-022-00961-5","DOIUrl":"https://doi.org/10.1007/s00281-022-00961-5","url":null,"abstract":"<p><p>Severe loss of cerebral blood flow causes hypoxia and glucose deprivation in the brain tissue, resulting in necrotic cell death in the ischemic brain. Several endogenous molecules, called alarmins or damage-associated molecular patterns (DAMPs), are extracellularly released from the dead cells to activate pattern recognition receptors (PRRs) in immune cells that infiltrate into ischemic brain tissue following the disruption of the blood-brain barrier (BBB) after stroke onset. The activated immune cells produce various inflammatory cytokines and chemokines, triggering sterile cerebral inflammation in the ischemic brain that causes further neuronal cell death. Poststroke inflammation is resolved within several days after stroke onset, and neurological functions are restored to some extent as neural repair occurs around peri-infarct neurons. Clearance of DAMPs from the injured brain is necessary for the resolution of poststroke inflammation. Neurons and glial cells also express PRRs and receive DAMP signaling. Although the role of PRRs in neural cells in the ischemic brain has not yet been clarified, the signaling pathway is likely to be contribute to stroke pathology and neural repair after ischemic stroke. This review describes the molecular dynamics, signaling pathways, and functions of DAMPs in poststroke inflammation and its resolution.</p>","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"45 3","pages":"427-435"},"PeriodicalIF":9.0,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9693350","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}
引用次数: 4
Thromboinflammatory challenges in stroke pathophysiology. 卒中病理生理学中的血栓炎性挑战。
IF 9 2区 医学
Seminars in Immunopathology Pub Date : 2023-05-01 DOI: 10.1007/s00281-023-00994-4
R D Szepanowski, S Haupeltshofer, S E Vonhof, B Frank, C Kleinschnitz, A I Casas
{"title":"Thromboinflammatory challenges in stroke pathophysiology.","authors":"R D Szepanowski,&nbsp;S Haupeltshofer,&nbsp;S E Vonhof,&nbsp;B Frank,&nbsp;C Kleinschnitz,&nbsp;A I Casas","doi":"10.1007/s00281-023-00994-4","DOIUrl":"https://doi.org/10.1007/s00281-023-00994-4","url":null,"abstract":"<p><p>Despite years of encouraging translational research, ischemic stroke still remains as one of the highest unmet medical needs nowadays, causing a tremendous burden to health care systems worldwide. Following an ischemic insult, a complex signaling pathway emerges leading to highly interconnected thrombotic as well as neuroinflammatory signatures, the so-called thromboinflammatory cascade. Here, we thoroughly review the cell-specific and time-dependent role of different immune cell types, i.e., neutrophils, macrophages, T and B cells, as key thromboinflammatory mediators modulating the neuroinflammatory response upon stroke. Similarly, the relevance of platelets and their tight crosstalk with a variety of immune cells highlights the relevance of this cell-cell interaction during microvascular dysfunction, neovascularization, and cellular adhesion. Ultimately, we provide an up-to-date overview of therapeutic approaches mechanistically targeting thromboinflammation currently under clinical translation, especially focusing on phase I to III clinical trials.</p>","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"45 3","pages":"389-410"},"PeriodicalIF":9.0,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10241149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9689716","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}
引用次数: 3
Differences in the post-stroke innate immune response between young and old. 年轻人和老年人中风后先天免疫反应的差异。
IF 9 2区 医学
Seminars in Immunopathology Pub Date : 2023-05-01 DOI: 10.1007/s00281-023-00990-8
Mattia Gallizioli, Maria Arbaizar-Rovirosa, David Brea, Anna M Planas
{"title":"Differences in the post-stroke innate immune response between young and old.","authors":"Mattia Gallizioli,&nbsp;Maria Arbaizar-Rovirosa,&nbsp;David Brea,&nbsp;Anna M Planas","doi":"10.1007/s00281-023-00990-8","DOIUrl":"https://doi.org/10.1007/s00281-023-00990-8","url":null,"abstract":"<p><p>Aging is associated to progressive changes impairing fundamental cellular and tissue functions, and the relationships amongst them through the vascular and immune systems. Aging factors are key to understanding the pathophysiology of stroke since they increase its risk and worsen its functional outcome. Most currently recognised hallmarks of aging are also involved in the cerebral responses to stroke. Notably, age-associated chronic low-grade inflammation is related to innate immune responses highlighted by induction of type-I interferon. The interferon program is prominent in microglia where it interrelates cell damage, danger signals, and phagocytosis with immunometabolic disturbances and inflammation. Microglia engulfment of damaged myelin and cell debris may overwhelm the cellular capacity for waste removal inducing intracellular lipid accumulation. Acute inflammation and interferon-stimulated gene expression are also typical features of acute stroke, where danger signal recognition by microglia trigger immunometabolic alterations underscored by lipid droplet biogenesis. Aging reduces the capacity to control these responses causing increased and persistent inflammation, metabolic dysregulation, and impaired cellular waste disposal. In turn, chronic peripheral inflammation during aging induces immunosenescence further worsening stroke-induced immunodepression, thus increasing the risk of post-stroke infection. Aging also alters gut microbiota composition inducing dysbiosis. These changes are enhanced by age-related diseases, such as atherosclerosis and type-II diabetes, that further promote vascular aging, predispose to stroke, and exacerbate brain inflammation after stroke. Current advances in aging research suggest that some age-associated alterations may be reversed. Future work will unravel whether such evolving anti-aging research may enable designing strategies to improve stroke outcome in the elderly.</p>","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"45 3","pages":"367-376"},"PeriodicalIF":9.0,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10279582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9706356","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}
引用次数: 4
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