B cells pulsed with Helicobacter pylori antigen efficiently activate memory CD8+ T cells from H. pylori-infected individuals

Azem, Josef; Svennerholm, Ann‐Mari; Lundin, Björn

doi:10.1016/j.clim.2005.09.011

Cited by 25 publications

(24 citation statements)

References 41 publications

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“…It has also been demonstrated that H. pylori-reactive CD8 ϩ T cells can be activated by B cells and DC that have been pulsed with H. pylori antigens in vitro. Furthermore, memory CD8 ϩ T cells sorted from peripheral blood of H. pylori-infected individuals were highly responsive to H. pylori urease (55). Additionally, clinical studies in children have revealed higher numbers of circulating CD8 ϩ CD45RO ϩ and CD4 ϩ CD45RO ϩ memory as well as NK cells upon infection with H. pylori (56).…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Infection in a Pig Model Is Dominated by Th1 and Cytotoxic CD8⁺T Cell Responses

et al. 2013

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Helicobacter pylori is the dominant member of the gastric microbiota and colonizes the stomach of more than 50% of the human population worldwide (1). H. pylori colonization usually does not cause illness, since 85% of infected people remain asymptomatic throughout life, but infection with strains bearing the cag (cytotoxin-associated gene) pathogenicity island can result in peptic ulcer disease, gastric lymphoma, and gastric adenocarcinoma, the second leading cause of cancer-related deaths, in 15% of infected individuals (2, 3). Conversely, there also is increasing evidence of H. pylori providing protection against esophageal and cardial pathologies (4-7), childhood asthma (8-10), childhood allergies (9, 11), and diabetes and obesity (12). This Gram-negative microaerophilic bacterium of the Epsilonproteobacteria has coevolved with humans for at least 50,000 years, indicating high adaptation capacity to the environmental niche of the human gastric mucosa and suggesting the ability to evade the immune system (13) through mechanisms that are incompletely understood. Infection with H. pylori in humans is associated mainly with a mucosal Th1 response, which is unsuccessful in clearing the bacteria from the stomach and can lead to more severe immunopathology (14). The pathogenicity of H. pylori is determined by various hostand pathogen-related factors, including the host's genetic background, age, and immune status and the bacterium's ability for antigenic variation, molecular mimicry, intracellular persistence, and expression of pathogenicity factors (15).Regulatory T (Treg) cells play a crucial role in H. pylori's ability to evade the immune system and persist in the gastric mucosa. Specifically, H. pylori can trigger a reprogramming of dendritic cells (DC) by downregulating major histocompatibility complex II (MHC-II) and inducing interleukin-10 (IL-10) and inhibiting IL-12 secretion, thereby inducing H. pylori-specific Treg cells (16)(17)(18). B cells also play a regulatory role by promoting IL-10 production in cocultured CD4 ϩ cells and subsequent conversion into a T T lymphocytes were found in the gastric epithelium and lamina propria (LP) of H. pylori-infected children with grade I to III gastritis (22, 23). Furthermore, the CD8 ϩ HLA-DR ϩ chronically activated memory T cell subset was expanded in peripheral blood of H. pylori-colonized children with duodenal ulcers (24), suggesting a role for CD8 ϩ T cells in H. pylori-mediated pathology. The majority of in vivo studies on the host responses to H. pylori are based on mouse models; however, in contrast to human

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Infection in a Pig Model Is Dominated by Th1 and Cytotoxic CD8⁺T Cell Responses

et al. 2013

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“…CD8 ϩ T-cell numbers reportedly increase in the stomachs of individuals infected (3,19). Hence, it would be interesting (i) to examine the gastric CD8 ϩ T cells found in GK 1.5 mice after H. pylori infection for antigen-specific activation and cytokine production, (ii) to investigate whether gastritis could be initiated after the adoptive transfer of CD8 ϩ T cells into lymphopenic hosts such as RAG Ϫ/Ϫ mice, and (iii) to examine the progression of H. pylori infection in mice deficient in CD8 ϩ T cells.…”

Section: In This Study We Examined the Immune And Inflammatory Respomentioning

confidence: 99%

CD8⁺T Cells Are Associated with Severe Gastritis inHelicobacter pylori- Infected Mice in the Absence of CD4⁺T Cells

et al. 2008

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Helicobacter pylori infection results in the development of chronic gastritis, and CD4؉ T cells are a major component of the gastric cellular infiltrate. To examine whether CD4 ؉ T cells are important in initiating and maintaining H. pylori-induced gastritis, mice deficient in CD4 ؉ T cells (B6.BM1.GK 1.5 mice [GK 1.5 mice]) were infected with H. pylori. We found that as in normal mice, H. pylori-specific antibodies, mostly of the immunoglobulin M isotype, developed in GK 1.5 mice but were unable to cure H. pylori infection. Further, while the stomachs of H. pylori-infected GK 1.5 mice were more heavily infiltrated with CD8؉ T cells and B cells, mice deficient in both CD4؉ and CD8 ؉ T cells developed mild inflammation comparable to the level observed for C57BL/6 mice. These observations suggest that CD4 ؉ T cells may play an important role in regulating or suppressing gastric CD8؉ T cells which, in the absence of CD4 ؉ T cells, may mediate more-severe disease. These studies have revealed a potentially important role for CD8 ؉ T cells in the gastric disease resulting from H. pylori infection.Helicobacter pylori colonizes approximately 50% of the world's population, resulting in persistent stomach inflammation in infected individuals (30). Chronic H. pylori gastritis can lead to the development of gastric and duodenal ulcers and, ultimately, gastric cancer (10, 14, 15). The growth of H. pylori is restricted to the stomach lumen and epithelium, a site poorly served by classical immune effectors, and the proximal duodenum, and successful attempts at bacterial eradication through therapeutic vaccination have not been achieved (29). Immunomodulation might provide an alternate means of reducing H. pylori-mediated disease through qualitative changes to the inflammation induced by chronic infection. Any rational attempt at immunomodulation will require a more complete understanding of the bacterial and host drivers of chronic inflammation and the cellular infiltrate which is characteristic of Helicobacter-associated gastritis. CD4 ϩ T cells are a major component of the gastric cellular infiltrate in both human and experimental animal models of H. pylori infection (5-7, 18, 27). Severe combined immunodeficiency (SCID) mice that receive adoptively transferred splenic CD4 ϩ T cells develop gastritis after Helicobacter infection, but mice which received splenocytes depleted of CD4 ϩ T cells do not (7,20). Hence, CD4ϩ T cells are believed to be fundamental to the initiation and maintenance of gastric inflammation. We aimed to examine the role of CD4 ϩ T cells with respect to both effector and regulatory function and to determine whether gastritis was dependent on infiltration by CD4 ϩ T cells. In this study, CD4ϩ T-cell-deficient mice were infected with H. pylori and examined for the development of gastritis. MATERIALS AND METHODSMice. Female C57BL/6 mice were reared under specific-pathogen-free conditions at the animal facility of the Department of Microbiology and Immunology, The University of Melbourne. Female B6.BM1.GK 1....

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“…The favorable participation of CD8+ T cells in the immune response to H. pylori infection showed that H. pylori colonization is associated with a greater numbers of CD8+ lymphocytes in crypt of epithelium. Their role in the local responses is the production of IFN-γ, with increased expression of major histocompatibility complex class II molecules in adjacent cells (120). Despite these immune mechanisms, H. pylori infection is not eliminated because the bacteria have a number of mechanisms are evaded or regulate by host responses.…”

Section: Inflammation Induced By H Pylori Is Important In Gastric Camentioning

confidence: 99%

Genetic Alterations in Gastric Cancer Associated with Helicobacter pylori Infection

et al. 2017

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Gastric cancer is a world health problem and depicts the fourth leading mortality cause from malignancy in Mexico. Causation of gastric cancer is not only due to the combined effects of environmental factors and genetic variants. Recent molecular studies have transgressed a number of genes involved in gastric carcinogenesis. The aim of this review is to understand the recent basics of gene expression in the development of the process of gastric carcinogenesis. Genetic variants, polymorphisms, desoxyribonucleic acid methylation, and genes involved in mediating inflammation have been associated with the development of gastric carcinogenesis. Recently, these genes (interleukin 10, Il-17, mucin 1, β-catenin, CDX1, SMAD4, SERPINE1, hypoxia-inducible factor 1 subunit alpha, GSK3β, CDH17, matrix metalloproteinase 7, RUNX3, RASSF1A, TFF1, HAI-2, and COX-2) have been studied in association with oncogenic activation or inactivation of tumor suppressor genes. All these mechanisms have been investigated to elucidate the process of gastric carcinogenesis, as well as their potential use as biomarkers and/or molecular targets to treatment of disease.

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B cells pulsed with Helicobacter pylori antigen efficiently activate memory CD8+ T cells from H. pylori-infected individuals

Cited by 25 publications

References 41 publications

Helicobacter pylori Infection in a Pig Model Is Dominated by Th1 and Cytotoxic CD8⁺T Cell Responses

Helicobacter pylori Infection in a Pig Model Is Dominated by Th1 and Cytotoxic CD8⁺T Cell Responses

CD8⁺T Cells Are Associated with Severe Gastritis inHelicobacter pylori- Infected Mice in the Absence of CD4⁺T Cells

Genetic Alterations in Gastric Cancer Associated with Helicobacter pylori Infection

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B cells pulsed with Helicobacter pylori antigen efficiently activate memory CD8+ T cells from H. pylori-infected individuals

Cited by 25 publications

References 41 publications

Helicobacter pylori Infection in a Pig Model Is Dominated by Th1 and Cytotoxic CD8+T Cell Responses

Helicobacter pylori Infection in a Pig Model Is Dominated by Th1 and Cytotoxic CD8+T Cell Responses

CD8+T Cells Are Associated with Severe Gastritis inHelicobacter pylori- Infected Mice in the Absence of CD4+T Cells

Genetic Alterations in Gastric Cancer Associated with Helicobacter pylori Infection

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Helicobacter pylori Infection in a Pig Model Is Dominated by Th1 and Cytotoxic CD8⁺T Cell Responses

Helicobacter pylori Infection in a Pig Model Is Dominated by Th1 and Cytotoxic CD8⁺T Cell Responses

CD8⁺T Cells Are Associated with Severe Gastritis inHelicobacter pylori- Infected Mice in the Absence of CD4⁺T Cells