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,
* Department of Biochemistry and Immunology and
School of Pharmacy, Federal University of Minas Gerais, Belo Horizonte, Brazil;
Centro de Pesquisas René Rachou, Fundacao Oswaldo Cruz, Belo Horizonte, Brazil;
Department of Parasitology, University of São Paulo, São Paulo, Brazil;
¶ Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037;
|| Discipline of Cell Biology, Federal University of São Paulo, São Paulo, Brazil; and
# Department of Molecular Biology, Princeton University, Princeton, NJ 08544
It has been proposed that self and protozoan-derived GPI anchors
are natural ligands of CD1d. In this study, we investigated the ability
of GPI anchors from Trypanosoma cruzi to bind to CD1d
and mediate activation of NKT cells. We observed that GPI-anchored
mucin-like glycoproteins (GPI mucins), glycoinositolphospholipids
(GIPLs), and their phosphatidylinositol moieties bind to rCD1d and
inhibit the stimulation of a NKT hybridoma by the
-galactosylceramide-CD1 complex. However, these GPI anchors and
related structures were unable to activate NKT cells in vitro or in
vivo. We found that high titers of Ab anti-GPI mucins, but not
anti-GIPLs, were detected in sera from wild-type as well as in
TAP1-/-, CD1d-/-, and MHC class
II-/- mice after immunization. However, T-dependent
anti-GPI mucin Ab isotypes, such as IgG1, IgG2a, IgG2b, and IgG3,
were absent on MHC class II-/-, but were conserved in
CD1d-/- and TAP1-/- mice. Furthermore, we
found that CD1d-/- mice presented a robust cytokine as
well as anti-GPI mucins and anti-GIPL Ab responses, upon
infection with T. cruzi parasites. These results
indicate that, despite binding to CD1d, GPI mucins and related
structures expressed by T. cruzi appear not to evoke
dominant CD1d-restricted immune responses in vivo. In contrast, MHC
class II is critical for the production of the major Ig G isotypes
against GPI mucins from T. cruzi
parasites.
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