REACTIVITY OF CHAGASIC ANTIGAL ANTIBODIES WITH NONINFECTED CELLS TREATED WITH TRYPANOSOMA-CRUZI SECRETED EXCRETED ANTIGENS/

Citation
Jku. Yokoyamayasunaka et al., REACTIVITY OF CHAGASIC ANTIGAL ANTIBODIES WITH NONINFECTED CELLS TREATED WITH TRYPANOSOMA-CRUZI SECRETED EXCRETED ANTIGENS/, Journal of clinical laboratory analysis, 12(2), 1998, pp. 108-114
Citations number
36
Categorie Soggetti
Medical Laboratory Technology
ISSN journal
08878013
Volume
12
Issue
2
Year of publication
1998
Pages
108 - 114
Database
ISI
SICI code
0887-8013(1998)12:2<108:ROCAAW>2.0.ZU;2-S
Abstract
Here, we show that antigal antibodies from Chagas' disease patients re act with noninfected host cells previously treated with antigens secre ted by the trypomastigote forms of Trypanosoma cruzi. With the excepti on of human and Old World monkey cells, which are GAL-negative, cells of all mammals express the GAL epitope (Gal alpha(1-3)Gal beta(1-4)Glc NAc-R) on their surface. Thus only the former ones develop antigal ant ibodies, Antigal antibodies increase during infection with T. cruzi, w hich expresses GAL epitopes on the surface of the infective forms. Her e, we show that, incubation of noninfected, GAL-negative cells with an tigens shed by T. cruzi renders these cells reactive to antigal antibo dies purified from chagasic sera. Neither chagasic sera depleted of an tigal antibodies nor antigal antibodies purified from normal sera disp lay reactivity with treated cells. Cell reactivity of chagasic antigal was abolished in the presence of melibiose (Gal alpha(1-6)Glc) or gal -gal (methyl 3-O-alpha-D-galactopyranosyl alpha-D-galactopyranoside). Since shedding of T. cruzi antigens can occur in vivo, these antigens may induce reactivity of chagasic antigal with noninfected human cells . The reactivity of noninfected, GAL-negative cells observed only with chagasic antigal antibodies can amplify the range of reactivity of th ese antibodies and consequently adds to their importance in the pathog enesis of human Chagas' disease. (C) 1998 Wiley-Liss, Inc.