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Infection and Immunity Mediated by the Carbohydrate Recognition Domain of theEntamoeba histolyticaGal/GalNAc Lectin
Author(s) -
James M. Dodson,
Paul W. Lenkowski,
Aleida C. Eubanks,
Terry F. G. H. Jackson,
Jason Napodano,
David M. Lyerly,
Lauren A. Lockhart,
Barbara J. Mann,
William A. Petri
Publication year - 1999
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/314610
Subject(s) - entamoeba histolytica , biology , lectin , microbiology and biotechnology , immune system , immunology , antibody , virology
Entamoeba histolytica causes invasive amebiasis, a major parasitic disease of the developing world, whose primary symptoms are liver abscess and colitis. All strains of E. histolytica express a 260-kDa surface Gal/GalNAc lectin that is antigenically conserved and immunogenic. The lectin is required for adherence to human intestinal epithelial cells and contact-dependent killing of immune effector cells. By expression cloning, the carbohydrate recognition domain (CRD) was identified within the lectin heavy-subunit cysteine-rich region. Of interest for a hepatic parasite, the CRD had sequence identity to the receptor-binding domain of hepatocyte growth factor (HGF) and competed with HGF for binding to the c-Met HGF receptor. In an animal model of invasive disease, immunization with the CRD inhibited liver-abscess formation, yet in humans, a naturally acquired immune response against the CRD did not persist.

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