| Literature DB >> 20865643 |
Woodruff Emlen1, Wenhan Li, Michael Kirschfink.
Abstract
Activation of the complement system significantly contributes to the pathogenesis of various acute and chronic inflammatory diseases. Current strategies to inhibit complement include the replacement or substitution of endogenous soluble complement inhibitors (e.g., C1 inhibitor [C1 inh], recombinant soluble complement receptor 1, TP10), the administration of antibodies to block key proteins of the cascade reaction (e.g., C5) or to neutralize the action of the complement-derived anaphylatoxins, or blockade of complement receptors (e.g., C5aR, CD88). The recent approvals of anti-C5 for the treatment of paroxysmal nocturnal hemoglobinuria as well as of C1 inh for the treatment of hereditary angioedema beyond European countries have provided a resurgence of interest in the potential of complement therapeutics for the treatment of disease. © Thieme Medical Publishers.Entities:
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Year: 2010 PMID: 20865643 DOI: 10.1055/s-0030-1262888
Source DB: PubMed Journal: Semin Thromb Hemost ISSN: 0094-6176 Impact factor: 4.180