Trypanosoma cruzi infection modulates in vivo expression of major histocompatibility complex class II molecules on antigen-presenting cells and T-cell stimulatory activity of dendritic cells in a strain-dependent manner.

ALBA SOTO, CATALINA D; MIRKIN, GERARDO A.; SOLANA, MARIA ELISA; GONZALEZ CAPPA, STELLA MARIS

INFECTION AND IMMUNITY

AMER SOC MICROBIOLOGY

Lugar: Washington; Año: 2003 vol. 71 p. 1194 - 1199

0019-9567

A striking feature of Chagas’ disease is the diversity of clinical presentations. Such variability may be due to the heterogeneity among T. cruzi isolates or to the host immune response. Employing two strains with opposite biological behavior, we investigated the effect of murine infection on professional antigen presenting cells (APC). Acute infection with the virulent RA strain down-regulated the constitutive expression of MHC class II in dendritic cells (DC) and inhibited its induction in peritoneal macrophages (PM) and splenic B cells. Infection with RA decreased splenic MHC class II mRNA levels and almost abrogated the ability of DC to prime allogeneic T cells and to form homotypic clusters, thus suggesting an impaired functionality of these cells. In contrast, the low virulence K98 strain maintained on DC, or stimulated on PM and B cells, the expression of MHC class II molecules and preserved DC´s T cell priming capacity and cluster formation. Both strains decreased CD86 expression on splenic DC at the acute stage. At the chronic phase, APC from survivors RA infected mice restored MHC class II expression to the levels found in K98 infection suggesting that infection with this virulent strain might cause a delay in the emergence of a specific immune response. Therefore, modulation of APC function is parasite strain-specific since infection with K98 strain induced their immunostimulatory potential while RA strain developed a mechanism to imbalance immune response by altering T cell activating capacity of APC.