ArticleThe American journal of pathology2009
Essential role for macrophage migration inhibitory factor in gastritis induced by Helicobacter pylori.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- Acyloxyacyl Hydrolase Protects against Kidney Injury via Inhibition of Tubular CD74-Macrophage Crosstalk.International journal of biological sciences · 2024Article
- [Precision Medicine for Gastric Cancer: Applicability from the Perspective ofThe Korean journal of helicobacter and upper gastrointestinal research · 2023Article
- Hsp90-stabilized MIF supports tumor progression via macrophage recruitment and angiogenesis in colorectal cancer.Cell death & disease · 2021Article
- Role of Host and Parasite MIF Cytokines duringTropical medicine and infectious disease · 2020Review
- Macrophage migration inhibitory factor as a potential prognostic factor in gastric cancer.World journal of gastroenterology · 2015Article
- Atherosclerosis following renal injury is ameliorated by pioglitazone and losartan via macrophage phenotype.Atherosclerosis · 2015Article
- Deletion of Smad3 improves cardiac allograft rejection in mice.Oncotarget · 2015Article
- Antral atrophy, intestinal metaplasia, and preneoplastic markers in Mexican children with Helicobacter pylori-positive and Helicobacter pylori-negative gastritis.Annals of diagnostic pathology · 2014Article
- Predictive computational modeling of the mucosal immune responses during Helicobacter pylori infection.PloS one · 2013Article
- Comparative analysis of the interaction of Helicobacter pylori with human dendritic cells, macrophages, and monocytes.Infection and immunity · 2012Article
- Nitric oxide modifies chromatin to suppress ICAM-1 expression during colonic inflammation.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Liver restores immune homeostasis after local inflammation despite the presence of autoreactive T cells.PloS one · 2012Article
- The role of Th cell subsets in the control of Helicobacter infections and in T cell-driven gastric immunopathology.Frontiers in immunology · 2012Article
- More than just a T-box: the role of T-bet as a possible biomarker and therapeutic target in autoimmune diseases.Immunotherapy · 2011Review
- Cathepsin X-deficient gastric epithelial cells in co-culture with macrophages: characterization of cytokine response and migration capability after Helicobacter pylori infection.The Journal of biological chemistry · 2010Article
- Human primary gastric dendritic cells induce a Th1 response to H. pylori.Mucosal immunology · 2010Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage migration inhibitory factor (MIF) is an upstream regulator of immune and inflammatory responses; however, its role in Helicobacter pylori (HP)-associated gastritis remains unknown. We infected MIF knockout (KO) and wild-type mice with SS1 HP and found that 2 weeks after infection, MIF and its receptor CD74 were markedly up-regulated in wild-type mice. This up-regulation preceded the up-regulation of both tumor necrosis factor-alpha and intercellular adhesion molecule-1, as well as the development of moderate gastritis at 8 weeks, as determined by a significant infiltration of neutrophils, T cells, and macrophages. In contrast, KO mice were protected against HP-induced gastritis by preventing the up-regulation of CD74 and Th1-mediated immune injury, including a reduction in the Th1 transcriptional factor T-bet and the expression of interferon-gamma. Additionally, inhibition of skin delayed type hypersensitivity reactions to HP antigens in KO mice also suggested a critical role for MIF in cell-mediated injury. A regulatory role for MIF in Th1-immune responses was further demonstrated by the finding that antigen-primed CD4(+) T cells lacking MIF failed to differentiate into the Th1 phenotype; these cells were instead promoted to Th2 differentiation after challenge with HP antigen in vitro. Results from this study indicated that inhibition of HP-induced innate immune responses and Th1-mediated immune injury may be the key mechanisms by which KO mice failed to develop gastritis after HP infection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.