ArticleInflammation2014
Mycobacterium leprae upregulates IRGM expression in monocytes and monocyte-derived macrophages.
Article in Inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 18 citations in OpenAlex.
- Xenophagy as a Strategy forPathogens (Basel, Switzerland) · 2023Review
- Immunity-related GTPase IRGM at the intersection of autophagy, inflammation, and tumorigenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- An increase in LRRK2 suppresses autophagy and enhances Dectin-1-induced immunity in a mouse model of colitis.Science translational medicine · 2018Article
- Innate Immune Responses in Leprosy.Frontiers in immunology · 2018Review
- Selective Autophagy and Xenophagy in Infection and Disease.Frontiers in cell and developmental biology · 2018Review
- Article
- Autophagy Is an Innate Mechanism Associated with Leprosy Polarization.PLoS pathogens · 2017Article
- Network Analysis of Human Genes Influencing Susceptibility to Mycobacterial Infections.PloS one · 2016Article
- Elevated expression of immunity-related GTPase family M in gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- IRGM governs the core autophagy machinery to conduct antimicrobial defense.Molecular cell · 2015Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leprosy is caused by the infection of Mycobacterium leprae, which evokes a strong inflammatory response and leads to nerve damage. Immunity-related GTPase family M protein (IRGM) plays critical roles in controlling inflammation. The objective of the study was to investigate whether IRGM is involved in the infection of M. leprae. Levels of IRGM were assessed in M. leprae-infected CD4(+) T cells, monocytes, and monocyte-derived macrophages. Data revealed that both protein and mRNA levels of IRGM were increased in monocytes after M. leprae infection. Interestingly, monocyte-derived macrophages showed more prominent IRGM expression with M. leprae infection, whereas the bacteria did not affect IRGM in CD4(+) T cells. Furthermore, we assessed levels of IRGM in CD4(+) T cells and monocytes from 78 leprosy patients and 40 healthy controls, and observed upregulated protein level of IRGM in the monocytes from leprosy patients. Also, IRGM expression was inversely correlated with the severity of the disease. These findings suggested a close involvement of IRGM in M. leprae infection and indicated a potential mechanism of defending M. leprae infection.
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Registered trials
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.