Biller et al. (2007) have, however, demonstrated increased expression of the mRNAs of FOXP3 and of the cytokines IL-10 and TGF-β in regulatory T cells (TReg) of dogs with cancer. In the present study, although specific cell populations such as TReg lymphocytes were not assessed, a positive correlation between the expression of FOXP3 and immunoregulatory (IL-10 and TGF-β) cytokines was confirmed (r = 0.6764/p < 0.001; r = 0.3151/p < 0.05, respectively). Additionally, low levels of FOXP3 expression were observed in the SD group compared with the AD and OD groups, and this was negatively correlated with clinical progression. check details Nevertheless, no

correlation between the up-regulation of IL-10 and TGF-β1 by FOXP3 and the clinical development of the disease could be observed. An explanation for this finding could be that FOXP3 is involved in regulating the expression of many

genes, as described in recent studies involving murine models ( Marson et al., 2007 and Zheng et al., 2007), or it might indicate that other cells could be involved in the production of these cytokines, how macrophages with the purpose of modulation of the immune response. It is, however, imperative that the role of FOXP3 in the development of regulatory cells in CVL be ascertained in future studies. Analysis of the cytokine profile with respect to parasite burden revealed increases in the expression of pro-inflammatory cytokines IFN-γ and TNF-α and in the transcription factor T-bet in all infected groups (LP, MP and HP) in comparison with the Metalloexopeptidase CD group (Fig. 2 and Fig. click here 4). T-bet is a key protein in the immune system and has been described as a TH1-specific T-box transcription factor controlling the development of TH1 cells and the expression

of the hallmark type 1 cytokine, IFN-γ, in TH1 and NK cells. A number of studies have established that T-bet plays an essential role in the control of TH1 cell-dependent protozoan infections (Rosas et al., 2006 and Szabo et al., 2002). Recently, Strauss-Ayali et al. (2007) reported an increase in T-bet and IFN-γ expression in experimentally and naturally infected dogs presenting parasite load in the spleen. In agreement with the present study, Lage et al. (2007) observed that, independent of the splenic parasitic load, levels of IFN-γ were significantly increased in naturally infected dogs compared with their non-infected counterparts. However, in contrast to the present study, no differences in the levels of TNF-α could be established between infected and non-infected dogs as previously described (Lage et al., 2007). Cytokines analysis considering dogs classified according clinical status revealed in AD group increases in IFN-γ, TNF-α (Fig. 1) and IFN-γ/IL-4 ratios in comparison with the SD and CD groups (CD: 0.32 ± 0.15; AD: 0.77 ± 0.50; OD: 0.80 ± 0.43, p < 0.05).