Molecular mechanisms of innate immune signal tranduction by the Toll-like receptor 4

A bacterial toxin called endotoxin triggers a devastating immune overreaction that kills roughly 135,000 people in Europe every year. The immune system normally recognises microbes and mounts a protective response—fever, fatigue, antibody production. But when certain bacteria release endotoxin (also called LPS) during severe infections, the same system can spiral into endotoxic shock, causing organ failure and death. Researchers do not fully understand why the same molecular trigger produces a beneficial reaction in one context and a lethal one in another. This project studies the molecular mechanisms by which immune cells detect endotoxin through the Toll-like receptor 4 and translate that signal into a cellular response. The goal is to map the precise biochemical steps that distinguish a normal, controlled immune response from a runaway pathological one. This is fundamental science. It will not produce a new drug or diagnostic test tomorrow. But understanding the molecular switch between protection and damage could eventually guide the design of therapies that dampen the dangerous side of the immune response without disabling its ability to fight infection—a balance that current treatments for sepsis and autoimmune diseases like rheumatoid arthritis and diabetes struggle to achieve.