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Toll-like receptors

Lien, Egil PhD; Ingalls, Robin R. MD


The ability of a host to sense invasion by pathogenic organisms and to respond appropriately to control infection is paramount to survival. In the case of sepsis and septic shock, however, an exaggerated systemic response may, in fact, contribute to the morbidity and mortality associated with overwhelming infections. The innate immune system has evolved as the first line of defense against invading microorganisms. The Toll-like receptors (TLRs) are a part of this innate immune defense, recognizing conserved patterns on microorganisms. These TLRs and their signaling pathways are represented in such diverse creatures as mammals, fruit flies, and plants. Ten members of the TLR family have been identified in humans, and several of them appear to recognize specific microbial products, including lipopolysaccharide, bacterial lipoproteins, peptidoglycan, and bacterial DNA. Signals initiated by the interaction of TLRs with specific microbial patterns direct the subsequent inflammatory response. Thus, TLR signaling represents a key component of the innate immune response to microbial infection.

From the Institute of Cancer Research and Molecular Biology (EL), Norwegian University of Science and Technology, University Medical Center, Trondheim, Norway; and the Department of Infectious Diseases (RRI), Boson Medical Center, Evans Biomedical Research Center, Boston, MA.

The innate immune system is the first line of defense against infection.

Supported, in part, by the Research Council of Norway, the Norwegian Cancer Society, and the Commission of the European Communities, specific RTD program “Quality of Life and Management of Living Resources,” QLK2-2000-00336, “Hospath” to (Dr. Lien), and National Institutes of Health grants R01 AI46613 and 5U19 AI38515 (to Dr. Ingalls).

Address requests for reprints to: Robin Ingalls, MD, Evans Biomedical Research Center, 650 Albany Street, 6th floor, Boston, MA 02118. E-mail:

© 2002 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins