Abstract Malaria infection elicits both protective and pathogenic immune responses, and IL‐27 is a critical cytokine that regulate effector responses during infection. Here, we identified a critical window of CD4 + T cell responses that is targeted by IL‐27. Neutralization of IL‐27 during acute infection with Plasmodium chabaudi expanded specific CD4 + T cells, which were maintained at high levels thereafter. In the chronic phase, Plasmodium‐ specific CD4 + T cells in IL‐27‐neutralized mice consisted mainly of CD127 + KLRG1 − and CD127 − KLRG1 + subpopulations that displayed distinct cytokine production, proliferative capacity, and are maintained in a manner independent of active infection. Single‐cell RNA‐seq analysis revealed that these CD4 + T cell subsets formed independent clusters that express unique Th1‐type genes. These IL‐27‐neutralized mice exhibited enhanced cellular and humoral immune responses and protection. These findings demonstrate that IL‐27, which is produced during the acute phase of malaria infection, inhibits the development of unique Th1 memory precursor CD4 + T cells, suggesting potential implications for the development of vaccines and other strategic interventions. IL‐27 inhibits the generation of parasite‐specific memory CD4 + T cells in a malaria infection model. Transient blockade of IL‐27 elicits high levels of unique CD127 + and KLRG1 + memory CD4 + T cells, elevates antibody production, and enhances protective immunity against secondary infection.
IL ‐27 produced during acute malaria infection regulates Plasmodium ‐specific memory CD4 + T cells
급성 말라리아 감염 중에 생성된 IL ‐27은 Plasmodium 특이적 기억 CD4 + T 세포를 조절합니다.
[Category] 말라리아,
[Source] pmc
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