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Sökning: LAR1:gu > Forskningsöversikt > Quiding Järbrink Marianne 1964

  • Resultat 1-9 av 9
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1.
  • Bergin, Philip, 1975, et al. (författare)
  • Secretion of matrix metalloproteinase-9 by macrophages, in vitro, in response to Helicobacter pylori.
  • 2005
  • Ingår i: FEMS immunology and medical microbiology. - : Oxford University Press (OUP). - 0928-8244 .- 1574-695X. ; 45:2, s. 159-69
  • Forskningsöversikt (refereegranskat)abstract
    • We have previously shown that matrix metalloproteinase-9 (MMP-9) activity is greatly enhanced within the active chronic inflammation of Helicobacter pylori infected individuals, of which a major fraction derives from macrophages in the tissue. Here, we have investigated the ability of macrophages to secrete MMPs in response to H. pylori. Human macrophages secrete MMP-9 in response to live and inactivated H. pylori, as well as to specific bacterial products. Protein kinase C, phosphatiolylinositol 3-kinase and calcium uptake channels all play a role in MMP-9 secretion, whereas neither tumour necrosis factor alpha, interleukin-8, nor interleukin-1beta autocrine stimulation appear to contribute. We conclude that human macrophages have the ability to react directly against several H. pylori derived factors, utilising several signalling pathways.
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2.
  • Enarsson, Karin, 1975, et al. (författare)
  • Differential mechanisms for T lymphocyte recruitment in normal and neoplastic human gastric mucosa
  • 2006
  • Ingår i: Clin Immunol. - : Elsevier BV. ; 118:1, s. 24-34
  • Forskningsöversikt (refereegranskat)abstract
    • Worldwide, gastric adenocarcinoma (GC) is the second most common cause of death from malignant disease. The reason why immune responses are unable to clear the tumour is not fully understood, although aberrant lymphocyte recruitment to the tumour site might be one factor. Therefore, we investigated the homing phenotype of mucosal T lymphocytes in GC, compared to tumour-free mucosa. We could detect significantly decreased frequencies of mucosal homing alpha4beta7+ T cells in the tumour tissues and increased frequencies of L-selectin+ T cells. This was probably due to the correlated decrease in MAdCAM-1 positive and increase in PNAd positive blood vessels in the tumour mucosa. There were also fewer CXCR3+ T lymphocytes in the tumour tissue. These findings provide evidence that endothelial cells within tumours arising at mucosal sites do not support extravasation of typical mucosa-infiltrating T cells. This may be of major relevance for future immunotherapeutic strategies for treatment of GC.
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3.
  • Enarsson, Karin, 1975, et al. (författare)
  • Helicobacter pylori induces transendothelial migration of activated memory T cells.
  • 2005
  • Ingår i: Infection and immunity. - 0019-9567. ; 73:2, s. 761-9
  • Forskningsöversikt (refereegranskat)abstract
    • Helicobacter pylori infection is associated with pronounced infiltration of granulocytes and lymphocytes into the gastric mucosa, resulting in active chronic gastritis that may develop into duodenal ulcer disease or gastric adenocarcinoma. Infiltrating T cells play a major role in the pathology of these diseases, but the signals involved in recruitment of T cells from blood to H. pylori-infected tissues are not well understood. We therefore examined H. pylori-induced T-cell transendothelial migration (TEM). The Transwell system, employing a monolayer of human umbilical vein endothelial cells, was used as a model to study TEM. H. pylori induced a significant T-cell migration, compared to spontaneous migration. CD4+ and CD8+ T cells migrated to the same extent in response to H. pylori, whereas there was significantly larger transmigration of memory T cells compared to naive T cells. Both H. pylori culture filtrate and urease induced migration, and the presence of the H. pylori cag pathogenicity island increased TEM. T-cell TEM was mediated by LFA-1-ICAM-1 interactions in accordance with an increased ICAM-1 expression on the endothelial cells after contact with H. pylori. Migrating T cells had increased expression of activation marker CD69 and chemokine receptors CXCR3, CCR4, and CCR9. Furthermore, T cells migrating in response to H. pylori secreted Th1 but not Th2 cytokines upon stimulation. In conclusion, our data indicate that live H. pylori and its secreted products contribute to T-cell recruitment to the gastric mucosa and that the responding T cells have an activated memory Th1 phenotype.
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4.
  • Hansson, Malin, 1967, et al. (författare)
  • Dendritic cells express CCR7 and migrate in response to CCL19 (MIP-3beta) after exposure to Helicobacter pylori
  • 2006
  • Ingår i: Microbes Infect. - : Elsevier BV. - 1286-4579. ; 8:3, s. 841-50
  • Forskningsöversikt (refereegranskat)abstract
    • Helicobacter pylori infection induces chronic inflammation in the gastric mucosa with a marked increase in the number of lymphoid follicles consisting of infiltrating B and T cells, neutrophils, dendritic cells (DC) and macrophages. It has been suggested that an accumulation of mature DC in the tissue, resulting from a failure of DC to migrate to lymph nodes, may contribute to this chronic inflammation. Migration of DC to lymph nodes is regulated by chemokine receptor CCR7, expressed on mature DC, and the CCR7 ligands CCL19 and CCL21. In this study we analysed the maturation, in vitro migration and cytokine production of human DC after stimulation with live H. pylori. For comparison, DC responses to non-pathogenic Escherichia coli bacteria were also evaluated. Stimulation with H. pylori induced maturation of DC, i.e. up-regulation of the chemokine receptors CCR7 and CXCR4 and the maturation markers HLA-DR, CD80 and CD86. The H. pylori-stimulated DC also induced CD4(+) T-cell proliferation. DC stimulated with H. pylori secreted significantly more interleukin (IL)-12 compared to DC stimulated with E. coli, while E. coli-stimulated DC secreted more IL-10. Despite low surface expression of CCR7 protein following stimulation with H. pylori compared to E. coli, the DC migrated equally well towards CCL19 after stimulation with both bacteria. Thus, we could not detect any failure in the migration of H. pylori stimulated DC in vitro that may contribute to chronic gastritis in vivo, and our results suggest that H. pylori induces maturation and migration of DC to lymph nodes where they promote T cell responses.
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5.
  • Lindholm, Catharina, 1967, et al. (författare)
  • Mucosal vaccination increases endothelial expression of mucosal addressin cell adhesion molecule 1 in the human gastrointestinal tract.
  • 2004
  • Ingår i: Infection and immunity. - 0019-9567. ; 72:2, s. 1004-9
  • Forskningsöversikt (refereegranskat)abstract
    • Homing of leukocytes to various tissues is dependent on the interaction between homing receptors on leukocytes and their ligands, addressins, on endothelial cells. Mucosal immunization results in homing of antigen-specific lymphocytes back to the mucosa where they first encountered the antigen. However, it is unknown whether this homing of antigen-specific cells is mediated by an altered endothelial addressin expression after vaccination. Using different immunization routes with an oral cholera vaccine, we show that the endothelial expression of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) is increased in the gastric and upper small intestinal mucosae after immunization through various local routes in the upper gastrointestinal tract. In contrast, rectal immunization did not influence the levels of MAdCAM-1 in the gastric or duodenal mucosa. Furthermore, we show that MAdCAM-1 can be induced on human endothelial cells by tumor necrosis factor alpha (TNF-alpha) and gamma interferon. The vaccine component cholera toxin B subunit (CTB) increased MAdCAM-1 expression on endothelial cells in cultured human gastric explants, an effect that seemed to be mediated by TNF-alpha. In conclusion, MAdCAM-1 expression is increased in the upper gastrointestinal tract after local immunizations with a vaccine containing CTB. This strongly suggests the involvement of MAdCAM-1 in the preferential homing of mucosal lymphocytes to their original site of activation.
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6.
  • Quiding-Järbrink, Marianne, 1964, et al. (författare)
  • Infections of the esophagus and the stomach.
  • 2009
  • Ingår i: Periodontology 2000. - : Wiley. - 1600-0757 .- 0906-6713. ; 49, s. 166-78
  • Forskningsöversikt (refereegranskat)
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7.
  • Raghavan, Sukanya, 1974, et al. (författare)
  • Immune modulation by regulatory T cells in Helicobacter pylori-associated diseases.
  • 2012
  • Ingår i: Endocrine, metabolic & immune disorders drug targets. - 2212-3873. ; 12:1, s. 71-85
  • Forskningsöversikt (refereegranskat)abstract
    • Regulatory T cells (Treg) have the ability to suppress the activity of most other lymphoid cells as well as dendritic cells through cell-cell contact dependent mechanisms, which have not yet been fully defined. Treg are a key component of a functional immune system, and Treg deficiency is associated with severe autoimmunity and allergies. Antigen-specific Treg accumulate in gastric tissue during both Helicobacter pylori-induced gastritis and peptic ulcer disease (PUD). Several studies suggest that the local Treg response protects the gastric mucosa from exaggerated inflammation and tissue damage, and the risk of PUD is inversely related to Treg frequencies. At the same time the reduction of the inflammatory response achieved by Treg leads to increased bacterial density. Furthermore, the inability to mount a protective inflammatory response will lead to chronic infection and in some patients to the development of atrophic gastritis and gastric cancer progression. Treg actively infiltrate gastric adenocarcinomas and are predicted to promote tumor escape from cytotoxic immune responses. In addition, the presence of a potent Treg response will probably be an obstacle when constructing a future therapeutic vaccine against H. pylori. In this article, we will review the proposed mechanisms of action for Treg, their accumulation in the gastric mucosa in the different H. pylori-associated diseases, and how they may affect the immune response induced by H. pylori infection and the course of PUD and gastric adenocarcinomas.
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8.
  • Raghavan, Sukanya, 1974, et al. (författare)
  • Regulatory T cells in gastrointestinal tumors
  • 2011
  • Ingår i: Expert Review of Gastroenterology & Hepatology. - 1747-4124. ; 5:4, s. 489-501
  • Forskningsöversikt (refereegranskat)abstract
    • Regulatory T cells (Tregs) have the ability to suppress the activity of most other lymphoid cells, as well as dendritic cells through cell-cell contact-dependent mechanisms, which have not yet been fully defined. Tregs are a key component of a functional immune system and Treg deficiency is associated with severe autoimmunity and allergies. However, Tregs specific for tumor-associated antigens are present in cancer patients and Tregs accumulate in many types of solid tumors, where they probably act to promote tumor escape from cytotoxic immune responses. Indeed, some studies even show a negative correlation between Treg infiltration and survival of the patient. Several studies indicate an active recruitment of Tregs to the tumor site and the mechanisms of Treg accumulation are starting to be better understood as a result of more detailed analysis of their adhesion molecule and chemokine receptor expression. In addition, in gastrointestinal tumors there is an increase in tumor-associated Tregs, but intriguingly, Treg infiltration into colorectal adenocarcinomas is associated with improved prognosis. In this article, we will review the proposed mechanisms of immune suppression by tumor-associated Tregs, how the tumor microenvironment favors immune evasion and Treg induction, the tumor-homing mechanisms of Tregs and how Tregs affect progression of gastric and colorectal tumors.
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  • Resultat 1-9 av 9

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