The C3a receptor, caspase-1, and release of IL-1ß.
Blood
; 122(20): 3394-5, 2013 Nov 14.
Article
em En
| MEDLINE
| ID: mdl-24235127
ABSTRACT
In this issue of Blood, Asgari et al report that engagement of the C3a receptor triggers interleukin-1b (IL-1b) processing and release via caspase-1 activation. The role of complement activation in IL-1 production has a long history; complement products function as "alarmins" during innate responses. For many years before the term "innate immune response" was coined, it was fully understood that a highly nonspecific event such as activation of complement would induce a highly nonspecific molecule such as IL-1; these 2 linked processes would then affect a highly specific event such antigen-driven lymphocyte activation, for example, polarization to a T helper 1 (Th1) or a Th17 response. In this issue, investigators link the generation of C3a to playing a role in the activation of caspase-1. A unique and unexpected finding of the study is that engagement of the C3a receptor results in phosphorylation of extracellular signal-regulated kinase-1 and 2 (ERK-1/2), which promotes the efflux of adenosine triphosphate (ATP) from the macrophage. Release of ATP is a rate-limiting step for activating caspase-1, as extracellular ATP triggers the P2X7 purinergic receptor to initiate oligomerization of NLRP3.
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Complemento C3
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Monócitos
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Proteínas de Transporte
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Trifosfato de Adenosina
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Interleucina-1beta
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Inflamassomos
Idioma:
En
Ano de publicação:
2013
Tipo de documento:
Article