期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2012
卷号：109
期号：30
页码：12129-12134
DOI：10.1073/pnas.1204480109
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Previous reports have shown that {gamma}{delta} T cells are important for the elimination of malaria parasites in humans and mice. However, how {gamma}{delta} T cells are involved in protective immunity against blood-stage malaria remains unknown. We infected {gamma}{delta} T-cell-deficient (TCR{delta}-KO) mice and control wild-type mice with Plasmodium berghei XAT, which is a nonlethal strain. Although infected red blood cells were eliminated within 30 d after infection, TCR{delta}-KO mice could not clear the infected red blood cells, showed high parasitemia, and eventually died. Therefore, {gamma}{delta} T cells are essential for clearance of the parasites. Here, we found that {gamma}{delta} T cells play a key role in dendritic cell activation after Plasmodium infection. On day 5 postinfection, {gamma}{delta} T cells produced IFN-{gamma} and expressed CD40 ligand during dendritic cell activation. These results suggest that {gamma}{delta} T cells enhance dendritic cell activation via IFN-{gamma} and CD40 ligand-CD40 signaling. This hypothesis is supported strongly by the fact that in vivo induction of CD40 signaling prevented the death of TCR{delta}-KO mice after infection with P. berghei XAT. This study improves our understanding of protective immunity against malaria and provides insights into {gamma}{delta} T-cell-mediated protective immunity against various infectious diseases.
