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Cellular and molecular mechanisms of intestinal fibrosis

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World Journal of Gastroenterology 2012年第28期18卷 3635-3661页

作者： Silvia Speca Ilaria Giusti Florian rieder Giovanni Latella Gastroenterology Unit Department of Internal Medicine and Public Health University of L'Aquila 67100 L'Aquila Italy Department of Gastroenterology and Hepatology Lerner Research Institute Cleveland Clinic Foundation Cleveland OH 73051 United States

Fibrosis is a chronic and progressive process characterized by an excessive accumulation of extracellular matrix (ECM) leading to stiffening and/or scarring of the involved tissue. Intestinal fibrosis may develop in several different enteropathies, including inflammatory bowel disease. It develops through complex cell, extracellular matrix, cytokine and growth factor interactions. Distinct cell types are involved in intestinal fibrosis, such as resident mesenchymal cells (fibroblasts, myofibroblasts and smooth muscle cells) but also ECM-producing cells derived from epithelial and endothelial cells (through a process termed epithelialand endothelial-mesenchymal transition), stellate cells, pericytes, local or bone marrow-derived stem cells. The most important soluble factors that regulate the activation of these cells include cytokines, chemokines, growth factors, components of the renin-angiotensin system, angiogenic factors, peroxisome proliferator-activated receptors, mammalian target of rapamycin, and products of oxidative stress. It soon becomes clear that although inflammation is responsible for triggering the onset of the fibrotic proc-ess, it only plays a minor role in the progression of this condition, as fibrosis may advance in a self-perpetuating fashion. Definition of the cellular and molecular mechanisms involved in intestinal fibrosis may provide the key to developing new therapeutic approaches.

关键词： Inflammatory bowel disease Intestinal fibrosis Extracellular matrix Molecular mediators Myofibroblasts Inflammatory cells Epithelial cells Mesenchymal cells Endothelial cells

H pylori infection causes chronic pancreatitis in Mongolian gerbils

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World Journal of Gastroenterology 2007年第29期13卷 3939-3947页

作者： Gabriele rieder Arno Karnholz Mechthild Stoeckelhuber Juanita L Merchant Rainer Haas Max von Pettenkofer-Institute for Hygiene and Medical Microbiology Ludwig-Maximilians-University 80336 Munich Germany Institute of Anatomy Ludwig- Maximilians-University 80336 Munich Germany University of Michigan Departments of Internal Medicine and Molecular and Integrative Physiology Ann Arbor Michigan United States

AIM： To investigate whether chronic H pylori infection has the potential to induce pancreatitis in the Mongolian gerbil model, and whether it is dependent on an intact type Ⅳ secretion system. METHoDS： Mongolian gerbils were infected with wild type （WT） H pylori type Ⅰ strain B128 or its isogenic mutant B128 △cag γ （defective type Ⅳ secretion）. After seven months of infection, H pylori was reisolated from antrum and corpus and Hpylori DNA was analyzed by seminested polymerase chain reaction （PCR）. Inflammation and histological changes were documented in the gastric antrum, corpus, and pancreas by immunohistochemistry. Cytokine mRNA, gastric pH, plasma gastrin, amylase, lipase, and glucose levels were determined. RESULTS： The H pylori infection rate was 95%. Eight infected animals, but none of the uninfected group, developed transmural inflammation and chronic pancreatitis. Extensive interstitial fibrosis and inflammation of the pancreatic lobe adjacent to the antrum was confirmed by trichrome stain, and immuno-histochemically. Pro-inflammatory cytokine mRNA was significantly increased in the antral mucosa of all infected gerbils. In the corpus, only cytokine levels of WT-infected animals andthose developing transmural inflammation and pancreatitis were significantly increased. Levels of lipase, but not glucose or amylase levels, were significantly reduced in the pancreatitis group. H pylori DNA was detected in infected antral and corpus tissue,but not in the pancreas CoNCLUSIoN： H pylori infection is able to induce chronic pancreatitis in Mongolian gerbils independently of the type Ⅳ secretion system, probably by an indirect mechanism associated with a penetrating ulcer.

关键词： H pylori Mongolian gerbil Pancreatitis Gastritis Penetrating ulcer

B7-H7 (HHLA2) inhibits T-cell activation and proliferation in the presence of TCR and CD28 signaling

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Cellular & Molecular Immunology 2021年第6期18卷 1503-1511页

作者： Sadiye Amcaoglu rieder Jingya Wang Natalie White Ariful Qadri Catherine Menard Geoffrey Stephens Jodi LKarnell Christopher ERudd Roland Kolbeck Present address:Viela Bio GaithersburgMDUSA Universite de Montreal MontrealQCCanada MedImmune/AstraZeneca GaithersburgMDUSA Biopharmaceuticals Early RIAAstraZenecaGaithersburgMDUSA Biopharmaceuticals Early RIAAstraZenecaGaithersburgMDUSA View author publications

Modulation of T-cell responses has played a key role in treating cancers and autoimmune ***,understanding how different receptors on T cells impact functional outcomes is *** influence of B7-H7(HHLA2)and CD28H(TMIGD2)on T-cell activation remains *** we examined global transcriptomic changes in human T cells induced by *** through TCR with oKT3 and B7-H7 resulted in modest fold changes in the expression of select genes;however,these fold changes were significantly lower than those induced by oKT3 and B7-1 *** transcriptional changes induced by oKT3 and B7-H7 were insufficient to provide functional stimulation as measured by evaluating T-cell proliferation and cytokine ***,B7-H7 was coinhibitory when simultaneously combined with TCR and CD28 *** inhibitory activity was comparable to that observed with ***,in physiological assays using T cells and APCs,blockade of B7-H7 enhanced T-cell activation and proliferation,demonstrating that this ligand acts as a break *** work defines that the transcriptomic changes induced by B7-H7 are insufficient to support full costimulation with TCR signaling and,instead,B7-H7 inhibits T-cell activation and proliferation in the presence of TCR and CD28 signaling.

关键词： T cell inhibition Checkpoint pathway T cell transcriptomics

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避免平幅衣片尺寸差异的途径和方法（二）

国外纺织技术（针织．服装分册） 1995年第5期 32-36页

作者： rieder,o 李炜

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避免平幅衣片尺寸差异的途径和方法（三）

国外纺织技术（针织．服装分册） 1996年第1期 12-17页

作者： rieder.o 李炜