**7. Acute and chronic infection**

78 Toxoplasmosis – Recent Advances

**5. Specific immune response** 

regulation of immune response [8].

**6. Humoral immune response** 

the parasite [6].

bradyzoites, which persist in tissue cyst for life. *T. gondii* is capable of triggering the nonspecific activation of macrophages and natural killer cells (NK-cells) along with other haematopoietic and non-haematopoietic cells. This activation is intended to limit parasite proliferation due to its direct or indirect cytotoxic action and to trigger a specific immune response due to the presentation of *T.* antigens. Non-specific response begins immediately following the first contact between the parasite and the host [5]. NK-cells take part in early phase of immune response. During the early phase of the infection, it is through the combined and synergetic action of the NK-cells and the macrophages, activated by IFN-γ. In activated macrophages vacuoles of lived tachyzoites merge with lysosomes and then follow out the destruction of parasites. Neutrophils and, very probably, eosinophils, and mast cells rapidly interfere to the infection and are involved in setting up a non-specific early immune

The non-specific immune response has led to differentiation of macrophages and Blymphocytes into antigen presenting cells. The effector cells are stimulated by dendritic cells presenting the antigen to T-lymphocytes. This mechanism requires a close interaction between the antigen presenting cell and the T-lymphocytes [7]. The interaction of parasite with mechanisms of non-specific immune response is important to orientation of progress of specific immunity. The induction of IL-12 and then IFN-γ stimulate the progression of Th1 subpopulations so that polarize the immune response for behoof cellular immunity. After acute infection, the cells presenting antigens (macrophages) are exciting to produce IL-12 and initiate differentiation of immature CD4 T-lymphocytes to Th1. The cellular immunity initiates the production of IFN-γ. This cytokine effects as a major mediator of cellular immunity during toxoplasmosis. The key function in specific immune response plays Tlymphocytes. These effector cells, which are involved in resistance to *T.* infection, then exert their function via a cytotoxic activity and/or the secretion of cytokines involved in the

CD4+ and CD8+ T-lymphocytes are the main players involved in resistance of the host to *T.*  infection CD4+ T-lymphocytes are required for the development of resistance during the early phase of the infection, and for immunity during vaccination. The CD8+ T-lymphocytes

Antibodies play a minor role but remain the essential means for diagnosing toxoplasmosis. The production of specific IgG antibodies usually begins 4 weeks after the infection and can continue for several months while the dynamics of antibody production does not yield substantial change during the course of disease. IgG are the second immunoglobulins to appear in toxoplasmosis. They play a role in protection of the foetus because they are capable of crossing the placenta. The main target antigens of IgG are the surface antigens of

exert a cytotoxic activity against tachyzoites or cells infected with *T. gondii* [9].

response *via* the production of IL-12 and various proinflammatory factors [6].

Cell-mediated immune responses are essential for host control of intracellular infections. *T. gondii* is a protozoan parasite that infects multiple vertebrate species and invades multiple cell types. Upon initial encounter with the immune system, the parasite rapidly induces production of the protective cytokine IL-12 most likely from a subpopulation of dendritic cells. NK and T-lymphocytes are then activated and triggered to synthesize IFN-γ, the major mediator of host resistance during the acute and chronic phases of infection. Cytokine (IFNγ and TNF-alpha) rather than cytotoxicity-based effector functions are more critical for protective immunity both during the acute and chronic phases of *T. gondii* infection. [10].

The T-lymphocytes, macrophages, and activity of interleukin IL-12 and IFN-γ is necessary for maintaining quiescence of chronic *T gondii* infection. IFN-γ stimulates anti-*T. gondii* activity, not only of macrophages, but also of nonphagocytic cells. TNF-alpha is another cytokine essential for control of chronic infection with *T. gondii* [11].
