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Milstein Lecture 2012: How do we sense microbes? From LPS, TNF, and the TLRs.

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Autoimmunity was conceptualized by Ehrlich, who posited more than 100 years ago that mechanisms for self/non-self discrimination must exist in any immune system. Today we know that recognition of non-self is exercised both by the innate and by the adaptive immune systems. Initial awareness of infection is provided by the former, and depends upon a remarkably small number of molecular interactions. In mammals, several types of innate immune sensors recognize conserved molecular signatures of infection, either on the surface of cells or within the cytosol. These sensors trigger a cytokine response that orchestrates inflammation, including the recruitment of many innate immune cells to the site of infection. Without this response, a state of immune compromise exists in which the host is quickly overwhelmed by microbes because it lacks awareness of infection. The Toll-like receptors (TLRs), an ancient family of innate immune sensors, are the most diverse in terms of ligand recognition. Their involvement in microbe sensing was discovered using a classical genetic approach. It was determined that one member of the TLR family, TLR4 , was mutated in mice that could not recognize bacterial lipopolysaccharide (LPS), known for many years as an inducer of systemic inflammation and shock during Gram-negative infection. The specificity of the other members of the TLR family was subsequently elucidated by reverse genetic methods. I will review these studies and consider TLR signaling pathways and the role played by TLRs in autoimmune and autoinflammatory diseases.

This talk is part of the MRC LMB Seminar list series.

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