Seminars in Immunology最新文献_第9页

The gut-brain vascular axis in neuroinflammation 神经性炎症中的肠-脑血管轴

IF 7.8 2区医学

Seminars in Immunology Pub Date : 2023-09-01 DOI: 10.1016/j.smim.2023.101802

Sara Carloni , Maria Rescigno

{"title":"The gut-brain vascular axis in neuroinflammation","authors":"Sara Carloni , Maria Rescigno","doi":"10.1016/j.smim.2023.101802","DOIUrl":"10.1016/j.smim.2023.101802","url":null,"abstract":"<div><p>The multifaceted microbiota characterizing our gut plays a crucial role in maintaining immune, metabolic and tissue homeostasis of the intestine as well as of distal organs, including the central nervous system. Microbial dysbiosis is reported in several inflammatory intestinal diseases characterized by the impairment of the gut epithelial and vascular barriers, defined as leaky gut, and it is reported as a potential danger condition associated with the development of metabolic, inflammatory and neurodegenerative diseases. Recently, we pointed out the strict connection between the gut and the brain via a novel vascular axis. Here we want to deepen our knowledge on the gut-brain axis, with particular emphasis on the connection between microbial dysbiosis, leaky gut, cerebral and gut vascular barriers, and neurodegenerative diseases. The firm association between microbial dysbiosis and impairment of the vascular gut-brain axis will be summarized in the context of protection, amelioration or boosting of Alzheimer, Parkinson, Major depressive and Anxiety disorders. Understanding the relationship between disease pathophysiology, mucosal barrier function and host-microbe interaction will foster the use of the microbiome as biomarker for health and disease as well as a target for therapeutic and nutritional advances.</p></div>","PeriodicalId":49546,"journal":{"name":"Seminars in Immunology","volume":"69 ","pages":"Article 101802"},"PeriodicalIF":7.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10157152","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: 3

Immune responses to SARS-CoV-2 infection and vaccination in children 儿童对SARS-CoV-2感染的免疫反应和疫苗接种

IF 7.8 2区医学

Seminars in Immunology Pub Date : 2023-09-01 DOI: 10.1016/j.smim.2023.101794

Petter Brodin

引用次数: 0

Pyroptosis-induced inflammation and tissue damage 焦热引起的炎症和组织损伤

IF 7.8 2区医学

Seminars in Immunology Pub Date : 2023-09-01 DOI: 10.1016/j.smim.2023.101781

Swathy O. Vasudevan , Bharat Behl , Vijay A. Rathinam

引用次数: 1

T cell fate decisions during memory cell generation with aging 记忆细胞衰老过程中的T细胞命运决定。

IF 7.8 2区医学

Seminars in Immunology Pub Date : 2023-09-01 DOI: 10.1016/j.smim.2023.101800

Ines Sturmlechner , Abhinav Jain , Yunmei Mu , Cornelia M. Weyand , Jörg J. Goronzy

{"title":"T cell fate decisions during memory cell generation with aging","authors":"Ines Sturmlechner , Abhinav Jain , Yunmei Mu , Cornelia M. Weyand , Jörg J. Goronzy","doi":"10.1016/j.smim.2023.101800","DOIUrl":"10.1016/j.smim.2023.101800","url":null,"abstract":"<div><p>The defense against infectious diseases, either through natural immunity or after vaccinations, relies on the generation and maintenance of protective T cell memory. Naïve T cells are at the center of memory T cell generation during primary responses. Upon activation, they undergo a complex, highly regulated differentiation process towards different functional states. Naïve T cells maintained into older age have undergone epigenetic adaptations that influence their fate decisions during differentiation. We review age-sensitive, molecular pathways and gene regulatory networks that bias naïve T cell differentiation towards effector cell generation at the expense of memory and Tfh cells. As a result, T cell differentiation in older adults is associated with release of bioactive waste products into the microenvironment, higher stress sensitivity as well as skewing towards pro-inflammatory signatures and shorter life spans. These maladaptations not only contribute to poor vaccine responses in older adults but also fuel a more inflammatory state.</p></div>","PeriodicalId":49546,"journal":{"name":"Seminars in Immunology","volume":"69 ","pages":"Article 101800"},"PeriodicalIF":7.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10528238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10169088","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

T follicular helper cells in cancer, tertiary lymphoid structures, and beyond T滤泡辅助细胞在癌症，三级淋巴结构，及其他

IF 7.8 2区医学

Seminars in Immunology Pub Date : 2023-09-01 DOI: 10.1016/j.smim.2023.101797

Can Cui , Joseph Craft , Nikhil S. Joshi

{"title":"T follicular helper cells in cancer, tertiary lymphoid structures, and beyond","authors":"Can Cui , Joseph Craft , Nikhil S. Joshi","doi":"10.1016/j.smim.2023.101797","DOIUrl":"10.1016/j.smim.2023.101797","url":null,"abstract":"<div><p>With the emergence and success of checkpoint blockade immunotherapy, immuno-oncology has primarily focused on CD8 T cells, whose cytotoxic programs directly target tumor cells. However, the limited response rate of current immunotherapy regimens has prompted investigation into other types of tumor-infiltrating immune cells, such as CD4 T cells and B cells, and how they interact with CD8 T cells in a coordinated network. Recent studies have demonstrated the potential therapeutic benefits of CD4 T follicular helper (TFH) cells and B cells in cancer, highlighting the important role of their crosstalk and interactions with other immune cell components in the tumor microenvironment. These interactions also occur in tumor-associated tertiary lymphoid structures (TLS), which resemble secondary lymphoid organs (SLOs) with orchestrated vascular, chemokine, and cellular infrastructures that support the developmental pathways of functional immune cells. In this review, we discuss recent breakthroughs on TFH biology and T cell-B cell interactions in tumor immunology, and their potential as novel therapeutic targets to advance cancer treatment.</p></div>","PeriodicalId":49546,"journal":{"name":"Seminars in Immunology","volume":"69 ","pages":"Article 101797"},"PeriodicalIF":7.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10156685","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

B cells and the intestinal microbiome in time, space and place B细胞与肠道菌群在时间、空间和地点上的关系

IF 7.8 2区医学

Seminars in Immunology Pub Date : 2023-09-01 DOI: 10.1016/j.smim.2023.101806

Oliver Pabst , Carla R. Nowosad

引用次数: 0

Microbial gasdermins: More than a billion years of pyroptotic-like cell death 微生物气胚层:超过十亿年的类似热腐的细胞死亡

IF 7.8 2区医学

Seminars in Immunology Pub Date : 2023-09-01 DOI: 10.1016/j.smim.2023.101813

Qi Zheng , Asen Daskalov

引用次数: 0

Pyroptosis and the cellular consequences of gasdermin pores Pyroposis和gasdermin毛孔的细胞后果。

IF 7.8 2区医学

Seminars in Immunology Pub Date : 2023-09-01 DOI: 10.1016/j.smim.2023.101803

Hanna C. Huston , Marisa J. Anderson , Susan L. Fink

引用次数: 0

Contributions of the early-life microbiome to childhood atopy and asthma development 早期生命微生物组对儿童特应性和哮喘发展的贡献

IF 7.8 2区医学

Seminars in Immunology Pub Date : 2023-09-01 DOI: 10.1016/j.smim.2023.101795

Holly Steininger , Jacqueline Moltzau-Anderson , Susan V. Lynch

{"title":"Contributions of the early-life microbiome to childhood atopy and asthma development","authors":"Holly Steininger , Jacqueline Moltzau-Anderson , Susan V. Lynch","doi":"10.1016/j.smim.2023.101795","DOIUrl":"10.1016/j.smim.2023.101795","url":null,"abstract":"<div><p>The rapid rise in atopy and asthma in industrialized nations has led to the identification of early life environmental factors that promote these conditions and spurred research into how such exposures may mediate the trajectory to childhood disease development. Over the past decade, the human microbiome has emerged as a key determinant of human health. This is largely due to the increasing appreciation for the myriad of non-mutually exclusive mechanisms by which microbes tune and train host immunity. Microbiomes, particularly those in early life, are shaped by extrinsic and intrinsic factors, including many of the exposures known to influence allergy and asthma risk. This has led to the over-arching hypothesis that such exposures mediate their effect on childhood atopy and asthma by altering the functions and metabolic productivity of microbiomes that shape immune function during this critical developmental period. The capacity to study microbiomes at the genetic and molecular level in humans from the pre-natal period into childhood with well-defined clinical outcomes, offers an unprecedented opportunity to identify early-life and inter-generational determinants of atopy and asthma outcomes. Moreover, such studies provide an integrative microbiome research framework that can be applied to other chronic inflammatory conditions. This review attempts to capture key studies in the field that offer insights into the developmental origins of childhood atopy and asthma, providing novel insights into microbial mediators of maladaptive immunity and chronic inflammatory disease in childhood.</p></div>","PeriodicalId":49546,"journal":{"name":"Seminars in Immunology","volume":"69 ","pages":"Article 101795"},"PeriodicalIF":7.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10166598","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: 1

Immune aging – A mechanism in autoimmune disease 免疫老化——自身免疫性疾病的一种机制

IF 7.8 2区医学

Seminars in Immunology Pub Date : 2023-09-01 DOI: 10.1016/j.smim.2023.101814

Yanyan Zheng , Qingxiang Liu , Jorg J. Goronzy , Cornelia M. Weyand

{"title":"Immune aging – A mechanism in autoimmune disease","authors":"Yanyan Zheng , Qingxiang Liu , Jorg J. Goronzy , Cornelia M. Weyand","doi":"10.1016/j.smim.2023.101814","DOIUrl":"10.1016/j.smim.2023.101814","url":null,"abstract":"<div><p>Evidence is emerging that the process of immune aging is a mechanism leading to autoimmunity. Over lifetime, the immune system adapts to profound changes in hematopoiesis and lymphogenesis, and progressively restructures in face of an ever-expanding exposome. Older adults fail to generate adequate immune responses against microbial infections and tumors, but accumulate aged T cells, B cells and myeloid cells. Age-associated B cells are highly efficient in autoantibody production. T-cell aging promotes the accrual of end-differentiated effector T cells with potent cytotoxic and pro-inflammatory abilities and myeloid cell aging supports a low grade, sterile and chronic inflammatory state (inflammaging). In pre-disposed individuals, immune aging can lead to frank autoimmune disease, manifesting with chronic inflammation and irreversible tissue damage. Emerging data support the concept that autoimmunity results from aging-induced failure of fundamental cellular processes in immune effector cells: genomic instability, loss of mitochondrial fitness, failing proteostasis, dwindling lysosomal degradation and inefficient autophagy. Here, we have reviewed the evidence that malfunctional mitochondria, disabled lysosomes and stressed endoplasmic reticula induce pathogenic T cells and macrophages that drive two autoimmune diseases, rheumatoid arthritis (RA) and giant cell arteritis (GCA). Recognizing immune aging as a risk factor for autoimmunity will open new avenues of immunomodulatory therapy, including the repair of malfunctioning mitochondria and lysosomes.</p></div>","PeriodicalId":49546,"journal":{"name":"Seminars in Immunology","volume":"69 ","pages":"Article 101814"},"PeriodicalIF":7.8,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10158130","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: 1