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Insufficient generation of Th17 cells in IL ‐23p19‐deficient BALB /c mice protects against progressive cutaneous leishmaniasis
Author(s) -
DietzeSchwonberg Kirsten,
Lorenz Beate,
Kostka Susanna Lopez,
Schumak Beatrix,
Gessner André,
Stebut Esther
Publication year - 2018
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13455
Subject(s) - balb/c , leishmania , immune system , immunology , leishmania major , leishmaniasis , interleukin 17 , cutaneous leishmaniasis , cytokine , interleukin 23 , interferon , disease , parasitic disease , interferon gamma , biology , medicine , parasite hosting , world wide web , computer science
Healing of leishmaniasis—a parasitic skin disease—is associated with high levels of secreted interferon ( IFN )γ and IL ‐12 in resistant C57 BL /6 mice and humans. Susceptible BALB /c mice predominantly react with a Th17/Th2/Treg‐related immune response and finally succumb to infection. Previously, we showed that BALB /c IL ‐17A −/− mice are protected against Leishmania (L.) major infections, indicating that IL ‐17A—predominantly produced by Th17 cells—plays an important role for disease outcome. We now investigated DC ‐derived cytokines and finally identified IL ‐23p19 as key cytokine responsible for induction of Leishmania ‐specific Th17 cells that play an important role for progressive disease in susceptible BALB /c mice.