Complement activation and inhibition: a delicate balance

Forskningsoutput: TidskriftsbidragÖversiktsartikel

Abstract

Complement is part of the innate immune defence and not only recognizes microbes but also unwanted host molecules to enhance phagocytosis and clearance. This process of opsonisation must be tightly regulated to prevent immunopathology. Endogenous ligands such as dying cells, extracellular matrix proteins, pentraxins, amyloid deposits, prions and DNA, all bind the complement activator C1q, but also interact with complement inhibitors Cob-binding protein and factor H. This contrasts to the interaction between C1q and immune complexes, in which case no inhibitors bind, resulting in full complement activation. Disturbances to the complement regulation on endogenous ligands can lead to diseases such as age-related macular degeneration, neurological and rheumatic disorders. A thorough understanding of these processes might be crucial to developing new therapeutic strategies.

Detaljer

Författare
Enheter & grupper
Forskningsområden

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Annan medicinsk grundvetenskap
Originalspråkengelska
Sidor (från-till)83-90
TidskriftTrends in Immunology
Volym30
Utgåva nummer2
StatusPublished - 2009
PublikationskategoriForskning
Peer review utfördJa