Preferentially expanding Vγ1+ γδ T cells are associated with protective immunity against Plasmodium infection in mice |
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Authors: | Shin‐Ichi Inoue Mamoru Niikura Hiroko Asahi Yoichiro Iwakura Yasushi Kawakami Fumie Kobayashi |
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Institution: | 1. Department of Infectious Diseases, Kyorin University School of Medicine, Tokyo, Japan;2. Research Institute for Biological Sciences, Tokyo University of Science, Chiba, Japan;3. Laboratory of Parasitology, School of Life and Environmental Science, Azabu University, Kanagawa, Japan |
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Abstract: | γδ T cells play a crucial role in controlling malaria parasites. Dendritic cell (DC) activation via CD40 ligand (CD40L)‐CD40 signaling by γδ T cells induces protective immunity against the blood‐stage Plasmodium berghei XAT (PbXAT) parasites in mice. However, it is unknown which γδ T‐cell subset has an effector role and is required to control the Plasmodium infection. Here, using antibodies to deplete TCR Vγ1+ cells, we saw that Vγ1+ γδ T cells were important for the control of PbXAT infection. Splenic Vγ1+ γδ T cells preferentially expand and express CD40L, and both Vγ1+ and Vγ4+ γδ T cells produce IFN‐γ during infection. Although expression of CD40L on Vγ1+ γδ T cells is maintained during infection, the IFN‐γ positivity of Vγ1+ γδ T cells is reduced in late‐phase infection due to γδ T‐cell dysfunction. In Plasmodium‐infected IFN‐γ signaling‐deficient mice, DC activation is reduced, resulting in the suppression of γδ T‐cell dysfunction and the dampening of γδ T‐cell expansion in the late phase of infection. Our data suggest that Vγ1+ γδ T cells represent a major subset responding to PbXAT infection and that the Vγ1+ γδ T‐cell response is dependent on IFN‐γ‐activated DCs. |
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Keywords: | CD40L Dendritic cells IFN‐γ Malaria Vγ 1+ γ δ T cells γ δ T cells γ δ T‐cell exhaustion |
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