AI Article Synopsis
- MTB, the bacteria that causes tuberculosis, uses specific proteins (MPT63 and MPT64) to evade the host's immune system and promote its survival.
- Researchers discovered that these proteins interact with key immune proteins (TBK1, p47phox, and HK2) and created a multifunctional recombinant protein (rMPT) that enhances immune responses and fights MTB.
- The study demonstrated that rMPT not only increases inflammation and reactive oxygen species but also shows potential as a vaccine or treatment against tuberculosis based on tests in mouse models.
Article Abstract
(MTB), the causative agent of tuberculosis (TB), avoids the host immune system through its virulence factors. MPT63 and MPT64 are the virulence factors secreted by MTB which regulate host proteins for the survival and proliferation of MTB in the host. Here, we found that MPT63 bound directly with TBK1 and p47phox, whereas MPT64 interacted with TBK1 and HK2. We constructed a MPT63/64-derived multifunctional recombinant protein (rMPT) that was able to interact with TBK1, p47phox, or HK2. rMPT was shown to regulate IFN-β levels and increase inflammation and concentration of reactive oxygen species (ROS), while targeting macrophages and killing MTB, both in vitro and in vivo. Furthermore, the identification of the role of rMPT against MTB was achieved via vaccination in a mouse model. Taken together, we here present rMPT, which, by regulating important immune signaling systems, can be considered an effective vaccine or therapeutic agent against MTB.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8152475 | PMC |
| http://dx.doi.org/10.3390/biomedicines9050545 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!