ArticleCurrent microbiology2008
Mycobacterium tuberculosis antigen Wag31 induces expression of C-chemokine XCL2 in macrophages.
Article in Current microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 12 citations in OpenAlex.
- Whole-Blood Gene Expression in Pulmonary Nontuberculous Mycobacterial Infection.American journal of respiratory cell and molecular biology · 2018Article
- Macrophage Immune Response Suppression by Recombinant Mycobacterium tuberculosis Antigens, the ESAT-6, CFP-10, and ESAT-6/CFP-10 Fusion Proteins.Iranian journal of medical sciences · 2016Article
- Structural and agonist properties of XCL2, the other member of the C-chemokine subfamily.Cytokine · 2015Article
- Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tuberculosis is still a major threat to human health. To date, only approximately half of the proteins encoded by Mycobacterium tuberculosis H37Rv have been assigned specific functions. Wag31 (Rv2145c) is one of the bacterial proteins whose function is mostly unknown. Using a modified split-ubiquitin membrane yeast two-hybrid system, we screened a macrophage cDNA library with Wag31 as bait and identified XCL2, a C-subfamily chemokine, as a binding partner for Wag31. More importantly, Wag31 was found to specifically stimulate XCL2 expression in macrophages. The results from this study demonstrate that expression of C-chemokine is not restricted to certain types of T cells and natural killer cells. Because C-chemokine is chemotactic for CD8+ and CD4+ T cells, our novel findings could provide a new mechanism by which the bacteria induce cell-mediated immunity and by which Wag31 could be a potential target for controlling M. tuberculosis 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.