Innate immunity and neural injury
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Head of Laboratory
Associate Professor Peter Crack+61 3 8344 8417
Project Details
A major new area of research in our laboratory is the role that the innate immune system plays in the progression of neural injury. It is now appreciated that the central nervous system (CNS) does exhibit features of inflammation, and in response to injury, infection or disease, resident CNS cells generate inflammatory mediators, including proinflammatory cytokines, prostaglandins, free radicals and complement, which in turn induce chemokines and adhesion molecules, recruit immune cells, and activate glial cells. Cerebral ischemia triggers acute inflammation, which exacerbates primary brain damage. Activation of the innate immune system is an important component of this inflammatory response. The innate immune system uses a newly discovered family of receptors to transducer its' signal called the Toll-like receptors (TLRs). The roll that the TLR's play in the progression and response to neural in jury is an exciting and emerging field of research. The molecular mechanisms that are influenced by the TLRs comprise new targets for therapeutic intervention into acute neurological conditions such as stroke and neurotrauma and chronic neurological diseases such as multiple sclerosis and Parkinsons disease.