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

Tan, Mai Ping; Pedersen, John; Zhan, Yifan; Lew, Andrew M.; Pearse, Martin J.; Wijburg, Odilia L. C.; Strugnell, Richard A.

doi:10.1128/iai.00779-07

Cited by 35 publications

(41 citation statements)

References 31 publications

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“…ϩ T cell responses to the bacterium have been detected only in immunodeficient mice lacking CD4 ϩ T cells (25,26). Results from these studies indicate that CD8 ϩ T cells also contribute to the development of gastric lesions, which traditionally has been attributed to effector CD4 ϩ T cells (27,28).…”

Section: H Pylori Infections Cd8mentioning

confidence: 70%

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: H Pylori Infections Cd8mentioning

confidence: 70%

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

et al. 2013

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“…7). In addition to NK-, NKT-and T H 1-polarized CD4 ϩ cells, CD8 ϩ T cells are known to be important producers of IFN-␥ during the adaptive phase of an immune response and have been implicated previously in Helicobacter-induced gastritis (51). We thus tested their possible contribution to Helicobacter clearance and associated immunopathology in our adoptive transfer model.…”

Section: Discussionmentioning

confidence: 99%

The CD4+ T Cell-Mediated IFN-γ Response to Helicobacter Infection Is Essential for Clearance and Determines Gastric Cancer Risk

Sayi

Kohler

Hitzler

et al. 2009

The Journal of Immunology

152

184

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“…More specifically, CD8+ T cell activity was found to be related to gastric inflammation during H. pylori infection [22].…”

Section: Discussionmentioning

confidence: 99%

IgG Subclasses Against Helicobacter pylori Isolates: An important Tool for Disease Characterization

et al. 2012

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Helicobacter pylori infects around 50% of the world’s population and is associated with diverse pathologies. In the most severe cases, the bacterium causes peptic ulcers and gastric cancer. The interplay between H. pylori and the host’s immune response may help to determine the specific outcome of the infection. To study the relationship between antibody subclasses and variation in immune recognition, we determined the immunoglobulin G1 and 2 (IgG1 and IgG2) titres of sera obtained from patients with different H. pylori‐associated pathologies. IgG1 and IgG2 titres were determined by ELISA in 44 sera of patients with different H. pylori‐associated diseases (peptic ulcer, bleeding peptic ulcers, gastric cancer and dyspepsia). Soluble proteins from lysates were obtained from 12 different clinical isolates from similar associated diseases. We found that soluble proteins from lysates of H. pylori strains (SPLHP) recognition patterns in these sera were highly variable. Overall, IgG2 titres were higher than the IgG1 titres in the infected patients. In particular, those with peptic ulcers showed marked elevation in IgG2/IgG1 ratios, while SPLHPs from dyspeptic patients resulted in high IgG1 titres. Our results reveal that correlation of antibody subclass titres with Th1/Th2 markers may aid pathology characterization and show a potential diagnosis that could be formally evaluated in other studies.

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

Cited by 35 publications

References 31 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

The CD4+ T Cell-Mediated IFN-γ Response to Helicobacter Infection Is Essential for Clearance and Determines Gastric Cancer Risk

IgG Subclasses Against Helicobacter pylori Isolates: An important Tool for Disease Characterization

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

Cited by 35 publications

References 31 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

The CD4+ T Cell-Mediated IFN-γ Response to Helicobacter Infection Is Essential for Clearance and Determines Gastric Cancer Risk

IgG Subclasses Against Helicobacter pylori Isolates: An important Tool for Disease Characterization

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Product

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

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