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The fever that accompanies many infections prompts production of heat-shock proteins, which protect cells from cold, heat and other stresses. Credit: Vicky Kasala Productions\/Getty<\/p>\n
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A fever fights infection by helping immune cells to crawl along blood-vessel walls to attack invading microbes.<\/p>\n
JianFeng Chen at the Shanghai Institute of Biochemistry and Cell Biology in China and his colleagues grew immune cells called T cells from mice, and raised the temperature of these cells from the normal mouse body temperature of 37 \u00b0C to 40 \u00b0C \u2014 the equivalent of a high fever. This heat triggered the T cells to start producing heat-shock proteins (Hsps), which protect cells against stress.<\/p>\n
The Hsps travelled to the inner surface of cells\u2019 outer membranes, where they bound to the tails of membrane proteins known as integrins. This process pulled integrins together, and the integrin sections jutting from the cells\u2019 outer surfaces formed complexes that stuck to blood-vessel walls. The formation of integrin complexes also triggered the migration of T cells to infection sites.<\/p>\n
The researchers then engineered mice to have a mutated form of integrin that couldn\u2019t bind to Hsps. When the team infected these animals with a diarrhoea-causing bacterium (Salmonella typhimurium<\/i>), the mice died quickly from fever and infection. The findings suggest that therapies designed to raise levels of Hsps could help to fight infection.<\/p>\n<\/div>\n