IL-27 plays an important role in expansion, differentiation, and mobilization of LSK cells to control malaria infection.

(A-D) Reduced induction of LSK cell population in WSX-1-deficient mice after malaria infection, accompanied by increased parasitemia and comparable production of IFN-γ. WT or WSX-1-deficient mice were infected with the blood stage of P. berghei XAT. Seven days later, parasitemia (A) and serum IFN-γ level (B) were determined, and LSK populations in the BM and spleen were analyzed by flow cytometry, and representative dot plots of c-Kit and Sca-1 in the Lin⁻ population are shown (C). Cell number of the LSK cell population was counted (D). (E) Augmented potential of LSK cells to differentiate into myeloid cells by malaria infection. LSK cells (1 × 10³) in the BM and spleen of the malaria-infected or non-infected WT mice were purified and differentiated into myeloid cells in vitro by IL-3 and SCF, and cell number of differentiated cells was counted. (F-G) Reduced cell number of neutrophils in WSX-1-deficient mice after malaria infection. The BM and spleen cells were analyzed for expression of Gr-1 and CD11b at 7 days after the infection (F), and cell number of neutrophils (Gr-1⁺CD11b⁺) was counted (G). (H-I) Decreased parasitemia in the WSX-1-deficient mice transferred with LSK cells purified from BM cells of the malaria-infected WT mice. LSK cells purified from BM cells of the infected WT CD45.1 mice were transferred into non-lethally irradiated WSX-1-deficient CD45.2 mice 7 days before infection. Neutrophil population in the BM and spleen was analyzed by flow cytometry, and representative dot plots of CD11b and Gr-1 in the CD45.1⁺ population are shown (H). Parasitemia was measured 4 and 7 days after the infection (I). Data are shown as mean ± SEM (n = 3–9) and are representative of at least two independent experiments. *P < 0.05, ***P < 0.005.