Welcome to the next installment of our regular update where we report on research from the world of immunology, highlighting work that has hit the headlines over the past few weeks.
RNA jelly acts as a vaccine for honey bees
Researchers from the University of Cambridge have discovered that honey bees are able to share immunity by transmitting RNA ‘vaccines’ through royal jelly and worker jelly. The ‘vaccines’ spread through the hive, suggesting the RNA fragments were being passed among individuals, generating herd immunity. In work published in Cell Reports, researchers fed bees RNA fragments that included a section of an RNA virus. They found that, similar to human vaccines, the dietary RNA activated an immune response in the bees that prevented disease and death when hives were later exposed to the live virus.
The vaccines persisted in multiple generations within the hive by being secreted in the jelly. Larvae that fed on the jelly inherited immunity in a manner similar to human babies who are breastfed. “We found that RNA spreads beyond individual honey bees, being transferred not just between parents and their progeny, but also among individuals in the hive,” says author Dr Eyal Maori of the Gurdon Institute, University of Cambridge.
The team found diverse types of RNA in the jelly, some derived from pathogenic viruses and fungi, suggesting that over time the bees had developed immunity against these pathogens, and shared it among the hive. The RNA was bound into granules to protect it from degradation. RNA granules have not been found to have a function outside cells before.
Protecting bees is important to maintain our food security and sustainability. These findings suggest a new way to shield bees from viruses and mites that have been responsible for dramatic declines in global honey bee populations.
Read the press release here
Read the full articles here: Maori et al. 2019 Cell Reports DOI: https://doi.org/10.1016/j.celrep.2019.04.073
Maori et al. 2019 Molecular Cell DOI: https://doi.org/10.1016/j.molcel.2019.03.010
MAC attack caught on camera
It is well-established that the membrane attack
complex (MAC) inserts in bacterial membranes to form pores that lead to the cells rupturing. For the first time, research led by University College London (UCL) and Imperial College London have caught the process on camera, in collaboration with the Swiss Federal Institute of Technology in Lausanne and the University of Leeds.
Published in Nature Communications, the study found that there was a pause after the pore began to form. Author Dr Edward Parsons from the London Centre for Nanotechnology at UCL said, “It appears as if these nanomachines wait a moment, allowing their potential victim to intervene in case it is one of the body’s own cells instead of an invading bug, before they deal the killer blow.” The authors suspect that the pause allows the body’s own cells to present a ‘self-marker’ to the MAC, preventing completion of the pore.
The team were able to see the MAC in such detail by combining multiple images using atomic force microscopy (AFM), where an ultrafine needle ‘feels’ rather than ‘sees’ molecules on a surface. This produces an image that refreshes fast enough to track how immune proteins connect to form the pore. The images were combined to show a movie of what happens over time. AFM images were then combined with structural data from cryo electron microscopy to determine how the structure changes as the pore is built.
Ancient protein is new drug target for Alzheimer's and cancer
SARM is an ancient immune protein that is one of the most conserved proteins of its type between worms, flies, and mammals. Researchers from Trinity College Dublin have discovered that SARM regulates inflammasomes, the molecular machines that trigger an inflammatory response to injury or infection.
The NLRP3 family of inflammasomes, which respond to danger signals such as viral DNA to initiate an inflammatory immune response, cause release of the inflammatory signal IL-1β. SARM regulates the inflammasome to stop this as a way of preventing an excessive immune response causing damage. When SARM was removed from the cell, more IL-1β was released, and cells became hyperactive rather than dying. As a result of reduced cell death, mice without SARM were protected from sepsis. When extra SARM was added to cells, it caused damage to mitochondria, the powerhouse of the cell, and lead to more cell death.
Professor Andrew Bowie, whose lab at Trinity College published the work in Immunity, said, "Scientists already knew that SARM drives cell death in the brain, and as a result it is being investigated as a therapeutic target for neurodegeneration and related diseases, but here we found that it is also a key immune regulator in peripheral immune cells.”
SARM regulates what happens to cells after inflammasome activation, controlling the balance between IL-1β production and cell death, potentially implicating SARM in regulation of inflammatory diseases . Researchers are hopeful that targeting SARM will allow them to regulate inflammation.