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• W2066369312 abstract "Chronically infected mice upregulate expression of inhibitory molecules on exhausted T cells. Harty and colleagues report similar findings in human patients with malaria and show that blockade of the inhibitory receptors PD-L1 and LAG-3 restores antimalaria responses in mice. Infection of erythrocytes with Plasmodium species induces clinical malaria. Parasite-specific CD4+ T cells correlate with lower parasite burdens and severity of human malaria and are needed to control blood-stage infection in mice. However, the characteristics of CD4+ T cells that determine protection or parasite persistence remain unknown. Here we show that infection of humans with Plasmodium falciparum resulted in higher expression of the inhibitory receptor PD-1 associated with T cell dysfunction. In vivo blockade of the PD-1 ligand PD-L1 and the inhibitory receptor LAG-3 restored CD4+ T cell function, amplified the number of follicular helper T cells and germinal-center B cells and plasmablasts, enhanced protective antibodies and rapidly cleared blood-stage malaria in mice. Thus, chronic malaria drives specific T cell dysfunction, and proper function can be restored by inhibitory therapies to enhance parasite control." @default.
• W2066369312 created "2016-06-24" @default.
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• W2066369312 date "2011-12-11" @default.
• W2066369312 modified "2023-10-05" @default.
• W2066369312 title "Therapeutic blockade of PD-L1 and LAG-3 rapidly clears established blood-stage Plasmodium infection" @default.
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• W2066369312 doi "https://doi.org/10.1038/ni.2180" @default.
• W2066369312 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3262959" @default.
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