| Literature DB >> 30144035 |
Shin-Ichi Inoue1,2, Mamoru Niikura2, Hiroko Asahi2, Yasushi Kawakami3, Fumie Kobayashi2,3.
Abstract
It is unclear whether γδ T cells are involved in humoral immunity against Plasmodium infection. Here, we show that B-cell-immunodeficient mice and γδ T-cell-deficient mice were incapable of protecting against Plasmodium berghei XAT parasites. γδ T-cell-deficient mice developed reduced levels of antigen-specific antibodies during the late phase of infection. The numbers of follicular helper T cells and germinal centre B cells in γδ T-cell-deficient mice were lower than in wild-type mice during the late phase of infection. Expression profiling of humoral immunity-related cytokines in γδ T cells showed that interleukin-21 (IL-21) and interferon-γ (IFN-γ) are increased during the early stage of infection. Furthermore, blockade of IL-21 and IFN-γ signalling during the early stage of infection led to reduction in follicular helper T cells and germinal centre B cells. γδ T-cell production of IL-21 and IFN-γ is crucial for the development and maintenance of follicular helper T cells and germinal centre B cells during the late phase of infection. Our data suggest that γδ T cells modulate humoral immunity against Plasmodium infection.Entities:
Keywords: humoral immunity; malaria; γδ T cells
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Year: 2018 PMID: 30144035 PMCID: PMC6231001 DOI: 10.1111/imm.12997
Source DB: PubMed Journal: Immunology ISSN: 0019-2805 Impact factor: 7.397