Knowing what turns off the molecular alarm system depends on our immune response.
Scientists have discovered what turns off the molecular alarm system, which plays a critical role in our immune response.
Antibacterial superhero MR1 (MHC molecule class I-related) is a protein found in all cells of the human body, which functions as a molecular alarm system, strong cells of our immune system, our white blood cells, with cancer or bacterial infection. present
While previous research has uncovered the cellular machinery that MR1 depends on to activate, there is no understanding of how the MR1 alarm is “turned off” until now.
Research co-led by Dr. Hamish McWilliam of the University of Melbourne and Jose Villadangos of the Doherty Institute and the Bio21 Institute Professor, in Journal of Cell Biology and reveals an essential molecular mechanism that regulates MR1 expression.
“What we found is that the protein – AP2 (adaptor protein 2) – inside our cells binds to MR1 and drags it inside the cells,” Dr. McWilliams interprets.
“Once inside, MR1 can no longer signal to white blood cells, which effectively turns off the immune response.”
In their experiments, the research team found that by deleting or mutating MR1 in AP2 cells, the activity of MR1 can be regulated, which in turn stimulates or inhibits the presence of white blood cells.
Dr. McWilliam says this is an exciting discovery as it unlocks a fundamental understanding of the biology of MR1 and contributes to global efforts to design immune boosting treatments.
“By understanding MR1, we could prevent or enhance the immune response, to control the immune system and the immune system to pathogens or tumors,” Dr. McWilliam says.
Reference: “Multiple tyrosine-based endocytosis signal in MR1 controlling antigen presentation to MAIT cells” Hui Jing Lim, Jacinta M. Wubben, Cristian Pinero Garcia, Sebastian Cruz-Gomez, Jieru Deng, Jeffrey YW Mak, Abderrahman Hachani, Regan J Anderson, Gavin F. Painter, Jesse Goyette, Shanika L. Amarasinghe, Matthew E. Ritchie, Antoine Roquilly, David P. Fairlie, Katharina Gaus, Jamie Rossjohn, Jose A. Villadangos and Hamish EG McWilliam, 21 September 2022; Journal of Cell Biology.
The study was funded by the National Health and Medical Research Council, Research Australia, the Australian Research Council, the Center of Excellence in Advanced Molecular Imaging, the National Institutes of Health, the New Zealand Ministry of Business Innovation and Employment, and the Horizon 2020 Framework Program.
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