Seminars in Immunopathology最新文献_第10页

Diseases of blood vessels: Immune system involvement in vasculitis and vasculopathy 血管疾病：免疫系统参与血管炎和血管病变

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-05-01 DOI: 10.1007/s00281-022-00929-5

P. Grayson, M. Kaplan

引用次数: 2

B cells in autoimmune hepatitis: bystanders or central players? 自身免疫性肝炎中的B细胞：旁观者还是中心参与者？

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-04-29 DOI: 10.1007/s00281-022-00937-5

C. Schultheiss, S. Steinmann, A. Lohse, M. Binder

引用次数: 11

Narcolepsy: a model interaction between immune system, nervous system, and sleep-wake regulation 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 : 2022-04-21 DOI: 10.1007/s00281-022-00933-9

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

引用次数: 10

COVID-19 Vasculitis and vasculopathy-Distinct immunopathology emerging from the close juxtaposition of Type II Pneumocytes and Pulmonary Endothelial Cells 新冠肺炎血管炎和血管病——II型肺细胞和肺内皮细胞紧密并置引起的免疫病理学

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-04-12 DOI: 10.1007/s00281-022-00928-6

S. Giryes, N. Bragazzi, C. Bridgewood, G. de Marco, D. McGonagle

引用次数: 12

Correction to: Cellular senescence in the cholangiopathies: a driver of immunopathology and a novel therapeutic target 更正：胆管疾病中的细胞衰老：免疫病理学的驱动因素和新的治疗靶点

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-03-31 DOI: 10.1007/s00281-022-00930-y

Christy E. Trussoni, S. O’Hara, N. LaRusso

引用次数: 1

Development of vascular disease models to explore disease causation and pathomechanisms of rare vascular diseases 建立血管疾病模型，探索罕见血管疾病的病因和发病机制

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-03-01 DOI: 10.1007/s00281-022-00925-9

R. Harper, Elisa A. Ferrante, M. Boehm

引用次数: 2

Chronoimmunology: from preclinical assessments to clinical applications. 时间免疫学：从临床前评估到临床应用

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-03-01 DOI: 10.1007/s00281-022-00923-x

Henrik Oster, David W Ray

引用次数: 0

Adaptive immunity, chronic inflammation and the clock. 适应性免疫，慢性炎症和生物钟。

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-03-01 DOI: 10.1007/s00281-022-00919-7

Kathryn J Gray, Julie E Gibbs

{"title":"Adaptive immunity, chronic inflammation and the clock.","authors":"Kathryn J Gray, Julie E Gibbs","doi":"10.1007/s00281-022-00919-7","DOIUrl":"https://doi.org/10.1007/s00281-022-00919-7","url":null,"abstract":"The adaptive arm of the immune system facilitates recognition of specific foreign pathogens and, via the action of T and B lymphocytes, induces a fine-tuned response to target the pathogen and develop immunological memory. The functionality of the adaptive immune system exhibits daily 24-h variation both in homeostatic processes (such as lymphocyte trafficking and development of T lymphocyte subsets) and in responses to challenge. Here, we discuss how the circadian clock exerts influence over the function of the adaptive immune system, considering the roles of cell intrinsic clockwork machinery and cell extrinsic rhythmic signals. Inappropriate or misguided actions of the adaptive immune system can lead to development of autoimmune diseases such as rheumatoid arthritis, ulcerative colitis and multiple sclerosis. Growing evidence indicates that disturbance of the circadian clock has negative impact on development and progression of these chronic inflammatory diseases and we examine current understanding of clock-immune interactions in the setting of these inflammatory conditions. A greater appreciation of circadian control of adaptive immunity will facilitate further understanding of mechanisms driving daily variation in disease states and drive improvements in the diagnosis and treatment of chronic inflammatory diseases.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"44 2","pages":"209-224"},"PeriodicalIF":9.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8901482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10851707","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: 21

Methods for statistical fine-mapping and their applications to auto-immune diseases. 统计精细绘图方法及其在自身免疫性疾病中的应用。

IF 7.9 2区医学

Seminars in Immunopathology Pub Date : 2022-01-01 Epub Date: 2022-01-18 DOI: 10.1007/s00281-021-00902-8

Qingbo S Wang, Hailiang Huang

引用次数: 0

Genetics of rheumatoid arthritis. 类风湿关节炎的遗传学。

IF 9 2区医学

Seminars in Immunopathology Pub Date : 2022-01-01 Epub Date: 2022-01-27 DOI: 10.1007/s00281-022-00912-0

Leonid Padyukov

{"title":"Genetics of rheumatoid arthritis.","authors":"Leonid Padyukov","doi":"10.1007/s00281-022-00912-0","DOIUrl":"https://doi.org/10.1007/s00281-022-00912-0","url":null,"abstract":"Rheumatoid arthritis (RA) is an inflammatory autoimmune disease involving symmetric joints and is generally characterized by persistent pain, tenderness, and destruction of joints. The vast majority of RA patients produce autoantibodies, and immune cell involvement in disease development is well recognized, as is the contribution of other types of cells in synovial tissue, like fibroblasts. It is known that there are major genetic associations with the HLA locus, while multiple non-HLA genetic variants display relatively low risk of RA. Both HLA and non-HLA associations suggest that the profiles of genetic associations for autoantibody-positive vs. autoantibody-negative RA are different. Several alleles of HLA-DRB1 are associated with high risk for autoantibody-positive RA, with the strongest risk characterized by valine at position 11 of the protein sequence (HLA-DRB1*04 and *10 alleles). There is a strong protective effect for the risk of autoantibody-positive RA associated with HLA-DRB1*13 alleles. Although major genetic associations have been known for several years, understanding of the specific mechanisms in the development of increased risk of RA for these variations is work in progress. Current studies focus on the binding of immune receptors involved in recognition of putative peptides in activation of T cells, as well as investigation of cell signaling mechanisms. At least a part of RA risk could be explained by gene-gene and gene-environment interactions. There are currently more than 150 candidate loci with polymorphisms that associate with RA, mainly related to seropositive disease, and new discoveries are anticipated in the future from investigation of diverse human populations. This new research will help create a strong foundation for the continuing process of integrating genetic, epigenetic, transcriptomic, and proteomic data in studies of RA.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"44 1","pages":"47-62"},"PeriodicalIF":9.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8837504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39728275","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: 35