CD4⁺T cells promote Plasmodium berghei blood-stage burden via IFN-γ secretion

Abstract Objective To investigate the role and mechanism of CD4⁺ T-cell-derived IFN-γ in host defense against blood-stage Plasmodium berghei (P. berghei) infection. Methods A tamoxifen-inducible conditional knockout strategy was performed to generate mice lacking IFN-γ specifically in CD4⁺T cells (Ifngfl/flCD4-CreERT2). Then after the mice were infected intravenously with luciferase-expressing P. berghei ANKA (P. berghei ANKA-luciferase) strain, parasite burden, survival, and intra-erythrocytic developmental rhythm were monitored dynamically. Flow cytometry and ELISA were carried out respectively to quantify the splenic myeloid subsets and the titers of P. berghei-specific IgG and IgG2c. Results CD4⁺T-cell-specific IFN-γ deficiency significantly reduced peripheral parasitemia on day 5 post-infection (P