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γδ T cells modulate humoral immunity against Plasmodium berghei infection
Author(s) -
Inoue ShinIchi,
Niikura Mamoru,
Asahi Hiroko,
Kawakami Yasushi,
Kobayashi Fumie
Publication year - 2018
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12997
Subject(s) - germinal center , biology , plasmodium berghei , immunology , humoral immunity , immunity , immune system , b cell , antigen , antibody , malaria
Summary 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.