In addition, sex hormones were reported to influence the activity of NK cells, which appeared to be critical in the early response to Neospora infection in calves [38, 39] and thus could have an additional impact on the reduction in immunity against N. caninum during pregnancy. However, the data on cytokine transcript expression shown here have been obtained at the end of the experiment and did not provide a clear picture on the timing of events during Selleckchem CX-4945 vaccination and challenge Infection. Thus, further studies are required to analyse the cytokine patterns at different time points

during vaccination and infection. In terms of controlling the infection by N. caninum in mice, there is no consensus on the roles of Th1 and Th2 cytokines. Vaccination of mice with native NcSRS2 induced a protective Th2-biased immune response against congenital infection [40].

In accordance with our results, others have suggested that a strong Th1 response may cause foetal death [41, 42] or enhance dissemination Galunisertib ic50 of the parasite by the lack of antibodies [43], which could explain the post-natal death of offspring. In other vaccination studies, high expression of the IFN-γ in vaccinated mice was associated with lack of protection against Neospora challenge [44, 45]. On the other hand, a strongly Th2-type biased immune response was also shown to be associated with exacerbation of the disease [46, 47]. A balanced Th1/Th2 response might confer the necessary protection, especially during pregnancy, to avoid allo-rejection of what is essentially a foreign graft [48]. A number of studies in cattle highlighted IKBKE the role of IFN-γ in mediating the pathological consequences of N. caninum infection, leading to foetal death [42, 49, 50]. However, the apparent dual function of IFN-γ

in Neospora infection to promote either pathology relating to foetal loss or inducing protective effects in terms of cerebral infection remains enigmatic. Multiple cytokines act synergistically, and each cytokine may change the action of one or several others [51]. Flynn and Marshall [52] suggested the major factor that could affect and drive the overall actions of IFN-γ during infection may be the proinflammatory mediator, IL-17A. The proinflammatory IL-17A cytokine and corresponding Th17 T cells developed from peripheral multipotent naïve CD4+ T-cell precursors (Th0) have been implicated in the pathogenesis of many infectious diseases, including those caused by the closely related T. gondii. The importance of CD4+ T cells populations for healthy pregnancy and the improper changes linked with adverse pregnancy has been demonstrated [53]. Regulatory T cells (Treg) described as CD4+CD25+Foxp3+ cells are also a subset of CD4+ T cells.