Seminars in Immunopathology最新文献_第9页

Correction to: Narcolepsy: a model interaction between immune system, nervous system, and sleep-wake regulation 更正：嗜睡症：免疫系统、神经系统和睡眠-觉醒调节之间的模型相互作用

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-26 DOI: 10.1007/s00281-022-00946-4

D. Latorre, F. Sallusto, C. Bassetti, U. Kallweit

引用次数: 3

The intestinal and biliary microbiome in autoimmune liver disease—current evidence and concepts 自身免疫性肝病的肠道和胆道微生物组——最新证据和概念

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-10 DOI: 10.1007/s00281-022-00936-6

T. Liwinski, Melina Heinemann, C. Schramm

引用次数: 20

Harnessing the liver to induce antigen-specific immune tolerance 利用肝脏诱导抗原特异性免疫耐受

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-05 DOI: 10.1007/s00281-022-00942-8

C. Gottwick, A. Carambia, J. Herkel

引用次数: 4

Glial-mediated neuroinflammatory mechanisms in age-related macular degeneration 年龄相关性黄斑变性的胶质细胞介导的神经炎症机制

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-05 DOI: 10.1007/s00281-022-00939-3

R. Dhodapkar, Diego Martell, B. Hafler

引用次数: 5

Cell death in development, maintenance, and diseases of the nervous system 神经系统发育、维持和疾病中的细胞死亡

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-04 DOI: 10.1007/s00281-022-00938-4

M. Mercau, Siraj Patwa, K. Bhat, Sourav Ghosh, C. Rothlin

引用次数: 2

Clonal hematopoiesis and vascular disease. 克隆造血和血管疾病。

IF 7.9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-01 Epub Date: 2022-02-04 DOI: 10.1007/s00281-022-00913-z

Kaushik Amancherla, John A Wells, Alexander G Bick

{"title":"Clonal hematopoiesis and vascular disease.","authors":"Kaushik Amancherla, John A Wells, Alexander G Bick","doi":"10.1007/s00281-022-00913-z","DOIUrl":"10.1007/s00281-022-00913-z","url":null,"abstract":"Somatic mutations in hematopoietic stem cells are common with aging and can result in expansion of clones harboring mutations, termed clonal hematopoiesis. This results in an increased risk of blood cancers but has also been linked with chronic inflammatory disease states. In recent years, clonal hematopoiesis has been established to have a causative role in atherogenesis and cardiovascular disease. Additionally, as the effector cells have been identified to be immune cells, there is ongoing interest in assessing whether dysregulated immune function plays a role in other chronic inflammatory conditions such as rheumatologic disease. Here, we summarize current understanding of clonal hematopoiesis with a focus on cardiovascular disease and inflammation while outlining the potential, yet unexplored, relationship between clonal hematopoiesis and autoimmune disease. Hematopoietic stem cells (HSCs) continually regenerate blood cells. Acquisition of a somatic mutation that provides a selective advantage, a driver mutation, can result in clonal expansion. Clonal hematopoiesis of indeterminate potential, where somatic mutations in certain cancer-associated genes result in clonal expansion in the absence of overt malignancy, can result in atherosclerotic cardiovascular disease in multiple vascular beds, inflammation, and may also contribute to the pathogenesis of autoimmune disease. Many questions remain unanswered regarding the relationship between clonal hematopoiesis and inflammatory disorders.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"44 3","pages":"303-308"},"PeriodicalIF":7.9,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9064918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9747206","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

Mechanisms of vascular damage in ANCA vasculitis. ANCA血管炎血管损伤的机制。

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-01 DOI: 10.1007/s00281-022-00920-0

David Massicotte-Azarniouch, Carolina A Herrera, J Charles Jennette, Ronald J Falk, Meghan E Free

{"title":"Mechanisms of vascular damage in ANCA vasculitis.","authors":"David Massicotte-Azarniouch, Carolina A Herrera, J Charles Jennette, Ronald J Falk, Meghan E Free","doi":"10.1007/s00281-022-00920-0","DOIUrl":"https://doi.org/10.1007/s00281-022-00920-0","url":null,"abstract":"The discovery of anti-neutrophil cytoplasmic antibodies (ANCA) and their antigenic targets, myeloperoxidase (MPO) and proteinase 3 (PR3), has led to further understanding as to the pathophysiologic processes that underlie vascular and tissue damage in ANCA vasculitis. ANCA trigger neutrophil activation leading to vascular damage in ANCA vasculitis. However, decades of study have determined that neutrophil activation alone is not sufficient to cause disease. Inflammatory stimuli are drivers of ANCA autoantigen expression and ANCA production. Certain infections or bacterial peptides may be crucial players in the initial steps of ANCA immunopathogenesis. Genetic and epigenetic alterations of gene encoding for MPO and PR3 provide additional disturbances to the immune homeostasis which provide a substrate for pathogenic ANCA formation from an adaptive immune system predisposed to autoreactivity. Promoted by inflammatory cytokines, ANCA binding leads to neutrophil activation, a process characterized by conformational changes, production and release of cytotoxic substances, and alternative complement pathway activation, thus creating an intense inflammatory milieu. This cascade of events perpetuates a vicious cycle of further inflammatory cell recruitment and activation, culminating in tissue necrosis. Our understanding of the pathogenic process in ANCA vasculitis paves the way for the development of therapies targeting crucial steps in this process. The greater appreciation of the role for complement, monocytes, and the adaptive immune system has already led to novel complement blockers and is poised to lead to further innovations which will allow for tailored antigen- or cell-specific immunotherapy targeting the autoimmune process without exposure to undue risks or toxicities.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"44 3","pages":"325-345"},"PeriodicalIF":9.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9064952/pdf/nihms-1789994.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9732568","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: 8

Age as a risk factor in vasculitis. 年龄是血管炎的危险因素。

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-01 DOI: 10.1007/s00281-022-00911-1

Andrea D Gloor, Gerald J Berry, Jorg J Goronzy, Cornelia M Weyand

{"title":"Age as a risk factor in vasculitis.","authors":"Andrea D Gloor, Gerald J Berry, Jorg J Goronzy, Cornelia M Weyand","doi":"10.1007/s00281-022-00911-1","DOIUrl":"https://doi.org/10.1007/s00281-022-00911-1","url":null,"abstract":"Two vasculitides, giant cell arteritis (GCA) and Takayasu arteritis (TAK), are recognized as autoimmune and autoinflammatory diseases that manifest exclusively within the aorta and its large branches. In both entities, the age of the affected host is a critical risk factor. TAK manifests during the 2nd-4th decade of life, occurring while the immune system is at its height of performance. GCA is a disease of older individuals, with infrequent cases during the 6th decade and peak incidence during the 8th decade of life. In both vasculitides, macrophages and T cells infiltrate into the adventitia and media of affected vessels, induce granulomatous inflammation, cause vessel wall destruction, and reprogram vascular cells to drive adventitial and neointimal expansion. In GCA, abnormal immunity originates in an aged immune system and evolves within the aged vascular microenvironment. One hallmark of the aging immune system is the preferential loss of CD8+ T cell function. Accordingly, in GCA but not in TAK, CD8+ effector T cells play a negligible role and anti-inflammatory CD8+ T regulatory cells are selectively impaired. Here, we review current evidence of how the process of immunosenescence impacts the risk for GCA and how fundamental differences in the age of the immune system translate into differences in the granulomatous immunopathology of TAK versus GCA.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"44 3","pages":"281-301"},"PeriodicalIF":9.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9064861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10802547","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: 18

Atherosclerosis and multi-organ-associated pathologies. 动脉粥样硬化和多器官相关病理。

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-01 DOI: 10.1007/s00281-022-00914-y

W Coles Keeter, Shelby Ma, Natalie Stahr, Alina K Moriarty, Elena V Galkina

{"title":"Atherosclerosis and multi-organ-associated pathologies.","authors":"W Coles Keeter, Shelby Ma, Natalie Stahr, Alina K Moriarty, Elena V Galkina","doi":"10.1007/s00281-022-00914-y","DOIUrl":"https://doi.org/10.1007/s00281-022-00914-y","url":null,"abstract":"Atherosclerosis is a chronic inflammatory disease of the vascular system that is characterized by the deposition of modified lipoproteins, accumulation of immune cells, and formation of fibrous tissue within the vessel wall. The disease occurs in vessels throughout the body and affects the functions of almost all organs including the lymphoid system, bone marrow, heart, brain, pancreas, adipose tissue, liver, kidneys, and gastrointestinal tract. Atherosclerosis and associated factors influence these tissues via the modulation of local vascular functions, induction of cholesterol-associated pathologies, and regulation of local immune responses. In this review, we discuss how atherosclerosis interferers with functions of different organs via several common pathways and how the disturbance of immunity in atherosclerosis can result in disease-provoking dysfunctions in multiple tissues. Our growing appreciation of the implication of atherosclerosis and associated microenvironmental conditions in the multi-organ pathology promises to influence our understanding of CVD-associated disease pathologies and to provide new therapeutic opportunities.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"44 3","pages":"363-374"},"PeriodicalIF":9.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9069968/pdf/nihms-1788782.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9435632","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: 11

Cardiovascular disease risk and pathogenesis in systemic lupus erythematosus. 系统性红斑狼疮的心血管疾病风险和发病机制。

IF 7.9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-01 Epub Date: 2022-03-30 DOI: 10.1007/s00281-022-00922-y

Christopher B Oliveira, Mariana J Kaplan

{"title":"Cardiovascular disease risk and pathogenesis in systemic lupus erythematosus.","authors":"Christopher B Oliveira, Mariana J Kaplan","doi":"10.1007/s00281-022-00922-y","DOIUrl":"10.1007/s00281-022-00922-y","url":null,"abstract":"Systemic lupus erythematosus (SLE) often features extensive cardiovascular (CV) comorbidity and patients with SLE are at significantly increased risk of CV event occurrence and CV-related mortality. While the specific mechanisms leading to this increased cardiovascular disease (CVD) risk remain to be fully characterized, this heightened risk cannot be fully explained by traditional CV risk factors and is likely driven by immunologic and inflammatory features of SLE. Widespread innate and adaptive immune dysregulation characterize SLE, and factors including excessive type I interferon burden, inappropriate formation and ineffective clearance of neutrophil extracellular traps, and autoantibody formation have been linked to clinical and metabolic features impacting CV risk in SLE and may represent pathogenic drivers of SLE-related CVD. Indeed, functional and phenotypic aberrations in almost every immune cell type are present in SLE and may impact CVD progression. As understanding of the contribution of SLE-specific factors to CVD in SLE improves, improved screening and monitoring of CV risk alongside development of therapeutic treatments aimed at prevention of CVD in SLE patients are required and remain the focus of several ongoing studies and lines of inquiry.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"44 3","pages":"309-324"},"PeriodicalIF":7.9,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9064999/pdf/nihms-1795694.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9436140","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