期刊
MOLECULAR AND BIOCHEMICAL PARASITOLOGY
卷 162, 期 2, 页码 105-111出版社
ELSEVIER
DOI: 10.1016/j.molbiopara.2008.08.006
关键词
Malaria; Inflammation; Toll-like receptor; Uric acid; Complement; Histamine
资金
- Canadian Institutes of Health Research (CIHR) [MT13721]
- Genome Canada through the Ontario Genomics Institute (KCK)
- CIHR Canada Research Chairs (WCL, KCK)
- Government of Canada Post-Doctoral Research Fellowship (CAMF)
- CIHR MD/PhD Studentship (LKE)
Severe forms of malaria infection claim over 1 million lives annually. One aspect of severe malaria pathogenesis is an excessive or dysregulated inflammatory response to infection. With the characterization of Toll-like receptors (TLRs), which initiate inflammation upon detection of microbial products, involvement of TLRs in the host response to malaria has undergone intense investigation. While TLRs appear to mediate inflammation in malaria infection and may contribute to development of severe malaria, it is unlikely that they operate in isolation from other components of innate immunity. Here, we highlight recent findings implicating other innate immune mechanisms in the host inflammatory response to malaria, propose how they may integrate and synergize with TLR pathways, and discuss opportunities and challenges associated with anti-inflammatory adjunctive therapy for the treatment of severe malaria. (C) 2008 Elsevier B.V. All rights reserved.
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