Abstract
The surface protein TIGIT (T cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif (ITIM) domain) has been characterized as an important regulator of cell-mediated immune responses in various infections. However, TIGIT expression in immune cells of mice infected with Toxoplasma gondii has not been investigated. Here, we detected TIGIT expression and related phenotypes by flow cytometry and real-time PCR in splenic and circulatory T cells of mice infected with the T. gondii RH strain. We found that the expression of TIGIT on the surface of CD4+ T cells and CD8+ T cells from the spleen and peripheral blood mononuclear cells decreased in the early stage, but increased significantly in the late stage of acute T. gondii infection in mice. Importantly, TIGIT expression was positively correlated with lesions in the murine spleen. In addition, T. gondii-specific TIGIT+TCM cells in the spleen were activated and transformed into TIGIT+ TEM cells. Hematoxylin and eosin staining of spleen sections and real-time PCR showed that the severity of splenic lesions was positively correlated with the T. gondii load. This study demonstrates that acute T. gondii infection can regulate the expression of TIGIT in T cells and affect immune cell function.
Highlights
The obligate intracellular parasitic protozoan Toxoplasma gondii (T. gondii) infects most warm-blooded animals and seriously threatens the health of human beings and animals [7, 20]
Compared with that of the control group, the TIGIT expression of CD4+ and CD8+T cells among peripheral blood mononuclear cells (PBMCs) of the infection group was significantly upregulated on the 7th day post infection (TIGIT+CD4+T cell: 5.58% ± 1.30% vs. 72.72% ± 0.64%, p < 0.001; TIGIT+CD8+T cells: 13.15% ± 2.32% vs. 78.72% ± 2.06%, p < 0.001)
TIGIT expression in T cell subsets within PBMCs and spleens from the infection group decreased on the third day post infection; this trend was more obvious in CD4+ T cells, but it only lasted until the fifth day after infection in CD4+T cells within PBMCs (Fig. 1)
Summary
The obligate intracellular parasitic protozoan Toxoplasma gondii (T. gondii) infects most warm-blooded animals and seriously threatens the health of human beings and animals [7, 20]. Transplacental or vertical transmission from the mother to the fetus occurs when tachyzoites pass through the placenta during pregnancy, or medical intervention When the immune function of the host is impaired, T. gondii will spread widely within the host via blood circulation and repeatedly invades and proliferates within host cells, resulting in damage to multiple organs and even death of the host [16]
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