Targeted complement inhibition and microvasculature in transplants: a therapeutic perspective.
Clin Exp Immunol
; 183(2): 175-86, 2016 Feb.
Article
en En
| MEDLINE
| ID: mdl-26404106
ABSTRACT
Active complement mediators play a key role in graft-versus-host diseases, but little attention has been given to the angiogenic balance and complement modulation during allograft acceptance. The complement cascade releases the powerful proinflammatory mediators C3a and C5a anaphylatoxins, C3b, C5b opsonins and terminal membrane attack complex into tissues, which are deleterious if unchecked. Blocking complement mediators has been considered to be a promising approach in the modern drug discovery plan, and a significant number of therapeutic alternatives have been developed to dampen complement activation and protect host cells. Numerous immune cells, especially macrophages, develop both anaphylatoxin and opsonin receptors on their cell surface and their binding affects the macrophage phenotype and their angiogenic properties. This review discusses the mechanism that complement contributes to angiogenic injury, and the development of future therapeutic targets by antagonizing activated complement mediators to preserve microvasculature in rejecting the transplanted organ.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Proteínas del Sistema Complemento
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Neovascularización Fisiológica
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Trasplantes
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Microvasos
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Rechazo de Injerto
Límite:
Humans
Idioma:
En
Revista:
Clin Exp Immunol
Año:
2016
Tipo del documento:
Article