ABSTRACT. A comparison of the expression of surface membrane antigens between dendritic cells (DC) derived from Peyer's patch macrophages (DPP-DC) of non-infected and Toxoplasma gondii (T. gondii) infected mice was performed. C57BL/6J mice aged 6-8 weeks of both sexes were infected orally with a 0.5 ml suspension containing 2 × 10 4 bradyzoites of the Beverley strain of T. gondii, sacrificed on day 8 and DC generated using discrete Peyer's patch macrophages (DPP-Mø) as progenitor cells. When a comparison of the expression of surface membrane antigens between the antigen presenting cells (APC) obtained from discrete Peyer's patches of non-infected and T. gondii infected mice was carried out, no significant differences were observed in the macrophage progenitor and DC populations expression of F4/80, DEC-205, CD11c, CD80 (B7-1) and CD34. However, a significant decrease in MHC class II antigen levels and a down regulation of the co-stimulatory molecule CD86 (B7-2) were noted. B7-1 appeared to be the dominant co-stimulatory ligand, whereas B7-2, which was down regulated during T. gondii infection, had a weak expression. Taken together, these results may help clarify the role of DC in the complex network regulating surface membrane antigens, as well as, their capacity for antigen uptake, processing and presentation during toxoplasmosis. Dendritic cells (DC) represent a rare population of antigen presenting cells (APC) in the blood, non-lymphoid and lymphoid tissues. They play a key role in the onset of cellular immunity and many studies have shown that DC capture, process and present antigen to memory and naive T cells [24][25][26][27]30]. The function of DC can be characterized by the dynamic regulation of differentiation/activation markers (CD83, CD25), of co-stimulatory molecules (CD40, CD80, CD86), and of class II major histocompatibility complexes (MHC class II) [14, 26-29, 31, 34].The major mechanism by which immuno-competent hosts control Toxoplasma gondii (T. gondii) infection is considered to be cell-mediated immunity [12]. The microbicidal or micro-biostatic activity of activated APC [40] and non-phagocytic cells [6,43] are the two major mechanisms of resistance to T. gondii infection. The physiologic regulation of Th phenotype development is still poorly understood, but because of the MHC class II restriction, attention has been focused on the major role of APC in the initiation of the immune response. In vitro studies have shown that activation of Th clones requires the presence of particular APC, i.e., DC or macrophages [8,33].High doses of the same soluble protein antigen given orally can result in non-responsiveness due to deletion or anergy of antigen-specific T cells [8], similar to what occurs following systemic administration of soluble proteins [33].However, not all oral encounters with antigen result in tolerance. Local and systemic T cell priming can occur when soluble antigens are administered with an ADP-ribosylating adjuvant, such as cholera toxin, which results in a Th2-dominant response, or...