The importance of <scp>TH</scp>22 and <scp>TC</scp>22 cells in the pathogenesis of <i>Helicobacter pylori‐</i>associated gastric diseases

Shamsdin, Seyedeh Azra; Alborzi, Abdolvahab; Rasouli, Manoochehr; Ghaderi, Abbas; Lankrani, Kamran B.; Dehghani, Seyed Mohsen; Pouladfar, Gholamreza

doi:10.1111/hel.12367

Cited by 11 publications

(10 citation statements)

References 25 publications

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“…Our outcomes indicated that TNF-α mRNA expression in H. pylori-infected patients was higher in comparison with that of H. pylori negative patients. These ndings are in agreement with previous reports that the TNF-α expression has been demonstrated to increase in the gastric mucosa of H. pylori-infected patients [31][32][33][34]. Several studies have demonstrated that polymorphisms in the TNF-α genes result in high transcriptional promoter activity along with increased gastric in ammation, which are related with an increased risk of H. pylorirelated GC and PUD developments [35,36].…”

Section: Discussionsupporting

confidence: 93%

“…In contrast to our detections, Shamsdin et al demonstrated that and noted no signi cant change in TNF-α serum levels in the infected patients with PUD and gastritis; however, the TNF-α serum levels in combination with IL-6 were found to be signi cantly higher in the gastritis patients as compared to the PUD patients. In addition, they observed signi cantly higher levels of TNF-α in the active chronic and chronic gastritis patients as compared to the uninfected groups [33].…”

Section: Discussionmentioning

confidence: 94%

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Relationship Between Mucosal TNF-α Expression and Th1, Th17, Th22 and Treg Responses in Helicobacter Pylori Infection

Rahimian

Abadi

Ahmadi

et al. 2021

Preprint

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Background: Helicobacter pylori (H. pylori) -induced gastric inflammation in the gastric mucosa and significantly increases the risk of developing gastritis and peptic ulcer disease (PUD). The objective of this research is to determine the role of tumor necrosis factor-α (TNF-α) expression in the gastric mucosa of patients with H. pylori –associated gastritis and PUD compared to uninfected patients, and we determined the relation between TNF-α expression and Th1/Th17/Th22, and Treg cells.Methods: Fifty-five patients with H. pylori –associated gastritis, 47 patients with H. pylori –associated PUD, and 48 uninfected patients were in this research. Antrum biopsy was used to detect H. pylori, virulence factors and histopathological assessments.Results: Expression of TNF-α in the infected group was significantly higher than the uninfected group. Also, cagA/oipA-positive infected patients induce significantly more TNF-α expression than do cagA/oipA-negative infected patients. Expression of TNF-α was significantly increased in the PUD group than the gastritis group. Notably, TNF-α expression had a significant positive correlation with the frequency of Th1/Th17/Th22 lymphocytes in the PUD group.Conclusion: These findings indicate the importance of increasing TNF-α with Th1, Th17, Th22 responses increase as an important risk factor for PUD in context of H. pylori infection.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 94%

Relationship Between Mucosal TNF-α Expression and Th1, Th17, Th22 and Treg Responses in Helicobacter Pylori Infection

Rahimian

Abadi

Ahmadi

et al. 2021

Preprint

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“…However, RA can enhance gap junction intercellular communication by increasing the expression of Cx43[126-128]. A previous study indicated that all-trans RA (ATRA) may inhibit gastric carcinoma tumor growth by targeting GC stem cells[129]; therefore, we predict that it may be mainly due to the effect of ATRA. The LPS-TLR4 signaling pathway has an important role in LPS-mediated disease.…”

Section: Cx43mentioning

confidence: 99%

How doesHelicobacter pyloricause gastric cancer through connexins: An opinion review

Gong

et al. 2019

WJG

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Helicobacter pylori (H. pylori) is a Gram-negative bacterium with a number of virulence factors, such as cytotoxin-associated gene A, vacuolating cytotoxin A, its pathogenicity island, and lipopolysaccharide, which cause gastrointestinal diseases. Connexins function in gap junctional homeostasis, and their downregulation is closely related to gastric carcinogenesis. Investigations into H. pylori infection and the fine-tuning of connexins in cells or tissues have been reported in previous studies. Therefore, in this review, the potential mechanisms of H. pylori-induced gastric cancer through connexins are summarized in detail.

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“…IL‐22‐producing T cells have previously been implicated in the pathogenesis of H. pylori infection . Shamsdin et al . analyzed subsets of IL‐22 + T cells in human peripheral blood mononuclear cells.…”

Section: Immunologymentioning

confidence: 99%

“…IL-22producing T cells have previously been implicated in the pathogenesis of H. pylori infection. 25 Shamsdin et al 26 Mezache et al 27 showed that PD-L1 is highly expressed in normal gastric mucosal biopsies and upregulated even further in H. pylori-infected tissue. The majority of PD-L1 + mononuclear cells were CD8 + , indicating that these cells play an important role in modulating the mucosal immune response.…”

Section: T Cells and Cytokinesmentioning

confidence: 99%

Helicobacter: Inflammation, immunology and vaccines

2017

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Helicobacter pylori is usually acquired in early childhood and the infection persists lifelong without causing symptoms. In a small of cases, the infection leads to gastric or duodenal ulcer disease, or gastric cancer. Why disease occurs in these individuals remains unclear, however the host response is known to play a very important part. Understanding the mechanisms involved in maintaining control over the immune and inflammatory response is therefore extremely important. Vaccines against H. pylori have remained elusive but are desperately needed for the prevention of gastric carcinogenesis. This review focuses on research findings which may prove useful in the development of prognostic tests for gastric cancer development, therapeutic agents to control immunopathology, and effective vaccines.

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The importance of TH22 and TC22 cells in the pathogenesis of Helicobacter pylori‐associated gastric diseases

Abstract: Increased Th22, Tc22, and Tc22/17 cells and IL-22 levels appear to be influential in progression and severity of H. pylori infection. Th22/17 can be an interesting therapeutic target for chronic H. pylori infections where eradication is more difficult.

Cited by 11 publications

References 25 publications

Relationship Between Mucosal TNF-α Expression and Th1, Th17, Th22 and Treg Responses in Helicobacter Pylori Infection

Relationship Between Mucosal TNF-α Expression and Th1, Th17, Th22 and Treg Responses in Helicobacter Pylori Infection

How doesHelicobacter pyloricause gastric cancer through connexins: An opinion review

Helicobacter: Inflammation, immunology and vaccines

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