ArticleClinical and experimental immunology2004
CTLA-4 blockade inhibits induction of Helicobacter pylori-associated gastritis in mice.
Article in Clinical and experimental immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Immunosuppression associated with chronic inflammation in the tumor microenvironment.Carcinogenesis · 2015Review
- Role of innate immunity in Helicobacter pylori-induced gastric malignancy.Physiological reviews · 2010Review
- Article
- CD4+ CD25+ regulatory T cells modulate the T-cell and antibody responses in helicobacter-infected BALB/c mice.Infection and immunity · 2006Article
- Effect of sucralfate on antibiotic therapy for Helicobacter pylori infection in mice.Antimicrobial agents and chemotherapy · 2004Article
- Severe Gastritis after Administration of Nivolumab and Ipilimumab.Case reports in oncologyArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The balance between Th1 and Th2 response determines the outcome of Helicobacter pylori infection. Interferon (IFN)-gamma plays an inductive role in gastric inflammation, whereas interleukin (IL)-4 counterbalances Th1 response and suppresses the development of gastritis. Th cell response is regulated by co-stimulatory factors. A co-stimulatory molecule, cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), plays an inhibitory role in IL-2-dependent cell growth and mediates an optimal inhibitory signal to Th1 and Th2 cells. We administered anti-CTLA-4 monoclonal antibody (MoAb), which blocks CTLA-4 signalling, to examine the relative role for this signalling during maturation of Th1 and Th2 cells in H. pylori infection in mice. Mice treated by anti-CTLA-4 MoAb within the first week of infection showed an inhibition of gastric inflammation, accompanied by an increasing ratio of H. pylori-specific IgG1/IgG2a in serum following infection. Furthermore, the treatment resulted in the higher ratio of IL-4/IFN-gamma by splenocytes in response to H. pylori antigen at 6 weeks after infection, compared with untreated mice. These results suggest that the predominance of Th2 response by CTLA-4 blockade leads to an inhibition of the development of gastric inflammation. CTLA-4 signalling could contribute to the regulation of Th subsets and the development of gastric inflammation in H. pylori infection.
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