Does Trypanosoma cruzi calreticulin modulate the complement system and angiogenesis?
Calreticulin, a calcium-binding protein that is highly conserved in its multiple functions, is present in a wide spectrum of subcellular compartments in virtually every cell of higher organisms. In this article, we propose a dual role for parasite calreticulin, with emphasis on the Trypanosoma cruzi model. By modulating the vertebrate complement system, calreticulin might provide the parasite with an effective immune-escape mechanism. Alternatively, by inhibiting angiogenesis, the parasite molecule might protect the host from ongoing neoplasic aggressions. Many questions are still unanswered, particularly those regarding the consequences that these interactions could have in vivo for both the parasite and the host.
Ferreira
Viviana
V
Programa de Inmunología, ICBM, Facultad de Medicina, Universidad de Chile, Independencia 1027, Santiago, Chile. aferreir@med.uchile.cl
Molina
María Carmen
MC
Schwaeble
Wilhelm
W
Lemus
David
D
Ferreira
Arturo
A
D043924:Angiogenesis Modulating Agents / Q000378:metabolism*; D000818:Animals; D037282:Calreticulin / Q000378:metabolism / Q000502:physiology*; D014355:Chagas Disease / Q000378:metabolism*; D003169:Complement Inactivator Proteins / Q000378:metabolism / Q000502:physiology*; D003165:Complement System Proteins / Q000378:metabolism; D006790:Host-Parasite Interactions / Q000502:physiology*; D006801:Humans; D014349:Trypanosoma cruzi / Q000378:metabolism*
D043924:Angiogenesis Modulating Agents; D037282:Calreticulin; D003169:Complement Inactivator Proteins; D003165:Complement System Proteins