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Clinical Implications of Basic Research
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Volume 348:167-169 January 9, 2003 Number 2
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Complement C5a in the Sepsis Syndrome — Too Much of a Good Thing?
Craig Gerard, Ph.D., M.D.

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In the sepsis syndrome, a "cytokine storm" unleashes numerous inflammatory mediators that contribute to multiple-organ dysfunction and, frequently, to death. During the past decade, research on how the innate immune system activates these mediators has led to remarkable discoveries, many of which are likely to affect the treatment of sepsis.

The pioneering work of Charles Janeway1 showed that the innate immune system recognizes pathogen-associated molecular patterns and, as a result, causes the release of powerful mediators that protect against infection. The toll family of receptors has emerged as a front-line mechanism by which cells recognize pathogen-associated molecular patterns in endotoxin, . . . [Full Text of this Article]


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From the Pulmonary Division, Children's Hospital, Boston.

Address reprint requests to Dr. Gerard at the Pulmonary Division, Children's Hospital, Enders Bldg., Rm. 144, 300 Longwood Ave., Boston, MA 02115, or at craig.gerard@tch.harvard.edu.


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