Dr Pete Monk in the Department of Infection, Immunity & Cardiovascular Disease provided an important component of a new study that provides the ‘missing link’ in the fight against bacterial infection, how a powerful part of the immune response becomes mobilised to fight invading bacteria. This was the first selective agonist for the second complement peptide 5a receptor (C5aR2), which was first isolated in Sheffield.
The article published in Science (17 June 2016 Volume 352 Issue 6292) was a collaborative effort from scientists across the world – Australia, UK, Ireland, USA, Germany.
T helper 1 immunity requires complement-driven NLRP3 inflammasome activity in CD4+ T cells
The classical view of immune activation is that innate immune cells, such as macrophages and dendritic cells, recognise invading microbes and then alert adaptive immune cells, such as T cells, to respond. Arbore et al. now show that innate and adaptive immunity converge in human and mouse T cells. Activated T cells express components of the complement cascade, which in turn leads to the assembly of NLRP3 inflammasomes — both critical components of innate immunity that help hosts detect and eliminate microbes. In T cells, complement and inflammasomes work together to push T cells to differentiate into a specialised subset of T cells important for eliminating intracellular bacteria.