A subset of liver NK T cells is activated during Leishmania donovani infection by CD1d-bound lipophosphoglycan Academic Article uri icon

Overview

MeSH Major

  • Antigens, CD1
  • Glycosphingolipids
  • Killer Cells, Natural
  • Leishmania donovani
  • Leishmaniasis, Visceral
  • Liver

abstract

  • Natural killer (NK) T cells are activated by synthetic or self-glycolipids and implicated in innate host resistance to a range of viral, bacterial, and protozoan pathogens. Despite the immunogenicity of microbial lipoglycans and their promiscuous binding to CD1d, no pathogen-derived glycolipid antigen presented by this pathway has been identified to date. In the current work, we show increased susceptibility of NK T cell-deficient CD1d(-/-) mice to Leishmania donovani infection and Leishmania-induced CD1d-dependent activation of NK T cells in wild-type animals. The elicited response was Th1 polarized, occurred as early as 2 h after infection, and was independent from IL-12. The Leishmania surface glycoconjugate lipophosphoglycan, as well as related glycoinositol phospholipids, bound with high affinity to CD1d and induced a CD1d-dependent IFNgamma response in naive intrahepatic lymphocytes. Together, these data identify Leishmania surface glycoconjugates as potential glycolipid antigens and suggest an important role for the CD1d-NK T cell immune axis in the early response to visceral Leishmania infection.

publication date

  • October 4, 2004

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2213292

Digital Object Identifier (DOI)

  • 10.1084/jem.20040704

PubMed ID

  • 15466622

Additional Document Info

start page

  • 895

end page

  • 904

volume

  • 200

number

  • 7