Objective  To explore the role and mechanism of γδ T cells in immune response of BALB/c mice infected with the lethal Plasmodium yoelii 17XL (P.y 17XL).

  Methods  Female BALB/c mice at 6 – 8 weeks of age were randomly divided into a normal control, P.y 17XL infection, and P.y 17XL infection and γδ T cell elimination group. The mice were intraperitoneally injected with P.y 17XL to infect 1×10⁶ red blood cells per mouse. The mice of γδ T cell elimination group were intraperitoneally injected with anti-mouse TCR γ/δ monoclonal antibody (150 μg/mouse) for two consecutive days before P.y 17XL infection, while the mice of normal control and P.y 17XL infection group were injected with the same volume of isotype control antibody. The infection rate of red blood cells and survival rate of mice were monitored dynamically. The number of γδ T cells, dendritic cells (DCs), and type 1 helper (Th1) cells in spleen cell suspension were detected with flow cytometry at the third and fifth day after P.y 17XL infection. After 48 hours′ cultivation in vitro, the supernatant specimens of spleen cell culture in vitro were collected for detections of interferon-γ (IFN-γ) and tumor necrosis factor α (TNF-α) with enzyme-linked immunosorbent assay (ELISA).

  Results  Compared with those of the normal control mice, the number of γδ T cells in spleen tissue of P.y 17XL infected mice increased significantly at the third and fifth day after the infection (both P < 0.05); while, the number of γδ T cells in spleen tissue of the mice with γδ T cell elimination decreased significantly (both P < 0.01). At the fifth day after the P.y 17XL infection, the number and activation of spleen DCs, the number of splenic Th1 cells, and the contents of IFN-γ and TNF-α in spleen cell culture supernatants increased significantly in mice with γδ T cell elimination in comparison with those in mice of P.y 17XL infection group.

  Conclusion  γδ T cells are involved in acute phase infection of P.y 17XL in erythrocytic stage. After γδ T cell elimination, the Th1 immune response increases as a compensation.