Evasion and Immuno-Endocrine Regulation in Parasite Infection: Two Sides of the Same Coin in Chagas Disease?

SILVINA R. VILLAR ; ALEXANDRE MORROT; ANA R. PEREZ; FLORENCIA B. GONZÁLEZ

Immune evasion strategies in protozoan-host interactions.

Frontiers Media SA

Lugar: Laussanne; Año: 2020; p. 156 - 165

Immune Evasion Strategies in Protozoan-Host InteractionsOne of the most successful protozoans is the malaria parasite, which has evolved key mechanisms toavoid the host immune system. This theme was recently reviewed with a focus on their capacity toovercome both innate responses, and the induction and maintenance of adaptive immune responses(Gomes, Bhardwaj et al.; Rénia and Goh; Gomes, Feijó et al.). With regards to this topic, the authorshighlighted the importance of carbohydrate-mediated interactions that directly affect Plasmodiumsurvival and host resistance. Plasmodium parasites have a complex life cycle in the vertebrate host.Initial stages comprise infection of hepatocytes, in which the CSP and TRAP domains of thesporozoite form of the parasite mediate an adhesive interaction with sulfated glycoconjugates on thesurface of hepatocytes, initiating the intracellular parasitism stage in the host. The dependency oncarbohydrate-mediated interactions for the parasitism also continues in the bloodstream form of theparasite via carbohydrates expressed by red blood cells, such as ABO, Lewis, and Duffy, whichthereby influences erythrocyte parasitism (Gomes, Feijó et al.).The glycobiology of parasite-host interactions has been proposed as a potential drug target. Thisis of particular importance for Chagas disease, a chronic infection caused by Trypanosoma cruzi.T. cruzi infection induces CD8 T cell responses able to control but not eliminate the parasite, whichis then able to subvert the host defenses via immuno-endocrine regulation (Cardoso et al.; Morrotet al.; Mendonça et al.; Silva-Neto et al.; Decote-Ricardo et al.; Sanmarco et al.; Gil-Jaramillo et al.).Drugs designed to interfere with carbohydrate-mediated interactions during host-pathogeninterplay have been shown to block the ability of T. cruzi to evade host immune surveillance.The parasite expresses a multifunctional enzyme called trans-sialidase responsible for catalyzing thetransfer of sialic acid domains from the host glycoconjugates to mucin-like molecules on the T. cruzicell surface. The sialylated domains of parasite mucins are shown to jeopardize host defenses,compromising both B and T cell-adaptive responses during infection (Nardy et al.; Freire-de-Lima et al.).The evasion strategies employed by Trypanosomadidae involve the modulation of componentsthat make up the large arsenal of defense mechanisms (cintinue....)NOTA: EL ADJUNTO ESTA TRUNCADO EN LA PAG 170, DEBIDO A QUE POR EL TAMAÑO DEL MISMO NO PODRIA CARGARSE EN SIGEVA.