Springer seminars in immunopathology最新文献_第7页

Mucosal T lymphocytes--peacekeepers and warriors. 粘膜T淋巴细胞——维和人员和战士。

Springer seminars in immunopathology Pub Date : 2005-09-01 Epub Date: 2005-06-02 DOI: 10.1007/s00281-005-0205-7

Hilde Cheroutre, Mitchell Kronenberg

引用次数: 13

Paneth cell alpha-defensins: peptide mediators of innate immunity in the small intestine. Paneth细胞α -防御素:小肠先天免疫的肽介质。

Springer seminars in immunopathology Pub Date : 2005-09-01 Epub Date: 2005-06-02 DOI: 10.1007/s00281-005-0202-x

Andre J Ouellette

{"title":"Paneth cell alpha-defensins: peptide mediators of innate immunity in the small intestine.","authors":"Andre J Ouellette","doi":"10.1007/s00281-005-0202-x","DOIUrl":"https://doi.org/10.1007/s00281-005-0202-x","url":null,"abstract":"Epithelial cells contribute to innate immunity by releasing antimicrobial peptides (AMPs) onto mucosal surfaces. In the small bowel, Paneth cells at the base of the crypts of Lieberkühn secrete alpha-defensins and additional AMPs at high levels in response to cholinergic stimulation and when exposed to bacterial antigens. The release of Paneth cell products into the crypt lumen is inferred to protect mitotically active crypt cells that renew the epithelial cell monolayer from colonization by potentially pathogenic microbes and to confer protection from enteric infection. The most compelling evidence for a Paneth cell role in enteric resistance to infection is evident from studies of mice transgenic for a human Paneth cell alpha-defensin, HD-5, which are completely immune to infection and systemic disease from orally administered Salmonella enterica serovar typhimurium. Cystic fibrosis mice are subject to small bowel bacterial overgrowth that is associated with impaired dissolution of released Paneth cell granules in the crypt lumen. Mutations that cause defects in the activation, secretion, dissolution, and bactericidal effects of Paneth cell AMPs may alter crypt innate immunity and contribute to immunopathology.","PeriodicalId":74860,"journal":{"name":"Springer seminars in immunopathology","volume":" ","pages":"133-46"},"PeriodicalIF":0.0,"publicationDate":"2005-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s00281-005-0202-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40943963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 67

Role of helminths in regulating mucosal inflammation. 蠕虫在调节粘膜炎症中的作用。

Springer seminars in immunopathology Pub Date : 2005-09-01 Epub Date: 2005-06-15 DOI: 10.1007/s00281-005-0209-3

Joel V Weinstock, Robert W Summers, David E Elliott

{"title":"Role of helminths in regulating mucosal inflammation.","authors":"Joel V Weinstock, Robert W Summers, David E Elliott","doi":"10.1007/s00281-005-0209-3","DOIUrl":"https://doi.org/10.1007/s00281-005-0209-3","url":null,"abstract":"The rapid rise in prevalence of ulcerative colitis (UC) and Crohn's disease (CD) in highly developed countries suggests that environmental change engenders risk for inflammatory bowel disease (IBD). Eradication of parasitic worms (helminths) through increased hygiene may be one such change that has led to increased prevalence of these diseases. Helminths alter host mucosal and systemic immunity, inhibiting dysregulated inflammatory responses. Animals exposed to helminths are protected from experimental colitis, encephalitis, and diabetes. Patients with CD or UC improve when exposed to whipworm. Lamina propria (LP) mononuclear cells from helminth-colonized mice make less interleukin (IL)-12 p40 and IFN-gamma, but more IL-4, IL-13, IL-10, TGF-beta, and PGE(2) compared to LP mononuclear cells from naive mice. Systemic immune responses show similar skewing toward Th2 and regulatory cytokine production in worm-colonized animal models and humans. Recent reports suggest that helminths induce regulatory T cell activity. These effects by once ubiquitous organisms may have protected individuals from many of the emerging immune-mediated illnesses like IBD, multiple sclerosis, type I diabetes, and asthma.","PeriodicalId":74860,"journal":{"name":"Springer seminars in immunopathology","volume":"27 2","pages":"249-71"},"PeriodicalIF":0.0,"publicationDate":"2005-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s00281-005-0209-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25138739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 65

Animal models of intestinal inflammation: ineffective communication between coalition members. 肠道炎症的动物模型:联盟成员之间的无效沟通。

Springer seminars in immunopathology Pub Date : 2005-09-01 Epub Date: 2005-07-19 DOI: 10.1007/s00281-005-0208-4

Robin G Lorenz, Vance J McCracken, Charles O Elson

引用次数: 25

The role of mucosal T lymphocytes in regulating intestinal inflammation. 粘膜T淋巴细胞在调节肠道炎症中的作用。

Springer seminars in immunopathology Pub Date : 2005-09-01 Epub Date: 2005-06-15 DOI: 10.1007/s00281-005-0206-6

Holm H Uhlig, Fiona Powrie

引用次数: 31

Intestinal mucosal responses to microbial infection. 肠道黏膜对微生物感染的反应。

Springer seminars in immunopathology Pub Date : 2005-09-01 Epub Date: 2005-06-01 DOI: 10.1007/s00281-005-0207-5

Lars Eckmann, Martin F Kagnoff

引用次数: 53

Gluten: a two-edged sword. Immunopathogenesis of celiac disease. 麸质:一把双刃剑。乳糜泻的免疫发病机制。

Springer seminars in immunopathology Pub Date : 2005-09-01 Epub Date: 2005-08-10 DOI: 10.1007/s00281-005-0203-9

Frits Koning, Luud Gilissen, Cisca Wijmenga

{"title":"Gluten: a two-edged sword. Immunopathogenesis of celiac disease.","authors":"Frits Koning, Luud Gilissen, Cisca Wijmenga","doi":"10.1007/s00281-005-0203-9","DOIUrl":"https://doi.org/10.1007/s00281-005-0203-9","url":null,"abstract":"Celiac disease (CD) is a small intestinal disorder caused by adaptive and innate immune responses triggered by the gluten proteins present in wheat. In the intestine, gluten is partially degraded and modified, which results in gluten peptides that bind with high affinity to HLA-DQ2 or HLA-DQ8 and trigger an inflammatory T cell response. Simultaneously, gluten exposure leads to increased production of IL15, which induces the expression of NKG2D on intraepithelial lymphocytes and its ligand MICA on epithelial cells, leading to epithelial cell destruction. The gluten-specific T cell response results in the production of antibodies against tissue transglutaminase and these are specific indicators of disease. CD is one of the most common inherited diseases, the HLA-DQ locus being the major contributing genetic factor. However, as the inheritance does not follow a Mendelian segregation pattern, multiple other genes, each with relative weak effect, contribute to disease development. An important role for environmental factors, however, can not be ignored as the concordance rate in monozygous twins is considerably less than 100%. The identification of these environmental factors and susceptibility genes may allow a better understanding of disease etiology and provide diagnostic and prognostic markers. The current treatment for CD consists of a life-long gluten-free diet. Although long thought to be impossible, recent results suggest that the development of nontoxic wheat varieties may be feasible, which would aid disease prevention and provide an alternative food source for patients.","PeriodicalId":74860,"journal":{"name":"Springer seminars in immunopathology","volume":"27 2","pages":"217-32"},"PeriodicalIF":0.0,"publicationDate":"2005-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s00281-005-0203-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25241738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 52

Pathogenesis of Helicobacter pylori infection. 幽门螺杆菌感染的发病机制。

Springer seminars in immunopathology Pub Date : 2005-09-01 Epub Date: 2005-06-01 DOI: 10.1007/s00281-005-0204-8

Richard M Peek

引用次数: 18

Immunopathology of the gastrointestinal system. Introduction. 胃肠系统的免疫病理学。介绍。

Springer seminars in immunopathology Pub Date : 2005-09-01 DOI: 10.1007/s00281-005-0210-x

Martin F Kagnoff

引用次数: 0

Cellular immunotherapy: antigen recognition is just the beginning. 细胞免疫疗法:抗原识别只是开始。

Springer seminars in immunopathology Pub Date : 2005-06-01 Epub Date: 2005-04-16 DOI: 10.1007/s00281-005-0200-z

Daniel S Chen, Mark M Davis

引用次数: 14