Unique T cells with unconventional cytokine profiles induced in the livers of mice during Schistosoma mansoni infection

PLoS One. 2013 Dec 16;8(12):e82698. doi: 10.1371/journal.pone.0082698. eCollection 2013.

Abstract

During infection with Schistosoma, serious hepatic disorders are induced in the host. The liver possesses unique immune systems composed of specialized cells that differ from those of other immune competent organs or tissues. Host immune responses change dramatically during Schistosoma mansoni infection; in the early phase, Th1-related responses are induced, whereas during the late phase Th2 reactions dominate. Here, we describe unique T cell populations induced in the liver of mice during the period between Th1- and Th2-phases, which we term the transition phase. During this phase, varieties of immune cells including T lymphocytes increase in the liver. Subsets of CD4(+) T cells exhibit unique cytokine production profiles, simultaneously producing both IFN-γ and IL-13 or both IFN-γ and IL-4. Furthermore, cells triply positive for IFN-γ, IL-13 and IL-4 also expand in the S. mansoni-infected liver. The induction of these unique cell populations does not occur in the spleen, indicating it is a phenomenon specific to the liver. In single hepatic CD4(+) T cells showing the unique cytokine profiles, both T-bet and GATA-3 are expressed. Thus, our studies show that S. mansoni infection triggers the induction of hepatic T cell subsets with unique cytokine profiles.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytokines / metabolism*
  • Female
  • Liver / immunology*
  • Liver / metabolism
  • Liver / pathology
  • Lymphocyte Count
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Schistosoma mansoni / immunology*
  • Schistosomiasis mansoni / immunology*
  • Schistosomiasis mansoni / metabolism*
  • Th1 Cells / metabolism*
  • Th1 Cells / pathology
  • Th2 Cells / metabolism*
  • Th2 Cells / pathology

Substances

  • Cytokines

Grants and funding

This work was supported by JSPS KAKENHI Grants-in-Aid for Scientific Research Number 24790402 (to K.A.), 25670204 (to S.H.), (http://www.jsps.go.jp/english/e-grants/index.html), a Health Labour Sciences Research Grant (H20-Shinkoh-Ippan-016, H23-Shinkoh-Ippan-014 to S.H.) (http://www.mhlw.go.jp/english/), and the Global COE Program, Nagasaki University, supported by MEXT (to S.H.) (http://www-sdc.med.nagasaki-u.ac.jp/gcoe/activities/publication/200901_e.html, http://www.jsps.go.jp/english/e-globalcoe/index.html). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.