IL-6 promotes CD4+ T-cell and B-cell activation during Plasmodium infection

Ismail Sebina, Lily Georgina Fogg, Kylie James, Megan Soon, Jasmin Akter, Bryce Thomas, Geoffrey Hill, Christian Engwerda, Ashraful Haque (Corresponding Author)

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

Abstract

Humoral immunity develops in the spleen during blood-stage Plasmodium infection. This elicits parasite-specific IgM and IgG, which control parasites and protect against malaria. Studies in mice have elucidated cells and molecules driving humoral immunity to Plasmodium, including CD4+ T cells, B cells, interleukin (IL)-21 and ICOS. IL-6, a cytokine readily detected in Plasmodium-infected mice and humans, is recognized in other systems as a driver of humoral immunity. Here, we examined the effect of infection-induced IL-6 on humoral immunity to Plasmodium. Using P. chabaudi chabaudi AS (PcAS) infection of wild-type and IL-6−/− mice, we found that IL-6 helped to control parasites during primary infection. IL-6 promoted early production of parasite-specific IgM but not IgG. Notably, splenic CD138+ plasmablast development was more dependent on IL-6 than germinal centre (GC) B-cell differentiation. IL-6 also promoted ICOS expression by CD4+ T cells, as well as their localization close to splenic B cells, but was not required for early Tfh-cell development. Finally, IL-6 promoted parasite control, IgM and IgG production, GC B-cell development and ICOS expression by Tfh cells in a second model, Py17XNL infection. IL-6 promotes CD4+ T-cell activation and B-cell responses during blood-stage Plasmodium infection, which encourages parasite-specific antibody production.
Original languageEnglish
Article numbere12455
JournalParasite Immunology
Volume39
Issue number10
Early online date17 Aug 2017
DOIs
Publication statusPublished - Oct 2017

Keywords

  • animal model
  • B lymphocyte
  • CD4 T lymphocyte
  • costimulatory molecules
  • cytokine
  • humoral immunity
  • malaria

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