Discovery of receptor-free signaling reveals better targets for treating autoimmune diseases

Our understanding of how cells interact with each other has been driven for decades by the central concept of receptor-mediated signal transduction. Now researchers from Boston Children's Hospital are reporting the discovery of a new, receptor-free means of signal transduction. This discovery not only suggests alternative pathways for cell-to-cell communication but also identifies a potentially more effective therapeutic target for treating autoimmune diseases. Their results are published today in Nature.

Jonathan Kagan, PhD, senior author and Director of Basic Research and Shwachman Chair in Gastroenterology, Boston Children'sThe discovery of this receptor-free signaling transduction underscores the value of exploratory science as a means to expand the lexicon of life."

Kagan and his team observed a different process wherein Toll-like Receptors (TLRs) – the guardians of our immune system – assembled but then released signaling proteins during the process of inflammation. Yet, contrary to dogma, the release of these signaling proteins did not stop the inflammatory process. Rather, the receptor-free state of these signaling proteins was necessary to assemble a key inflammation-stimulatory organelle called the myddosome. Without receptor release, myddosomes could not form nor induce inflammatory gene expression.

Source:

Boston Children's Hospital

Journal reference: