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IL‐1 signalling is dispensable for protective immunity in Leishmania ‐resistant mice
Author(s) -
KautzNeu Kordula,
Kostka Susanna L.,
Dinges Stephanie,
Iwakura Yoichiro,
Udey Mark C.,
von Stebut Esther
Publication year - 2011
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/j.1600-0625.2010.01172.x
Subject(s) - leishmania , immunology , leishmaniasis , leishmania major , cutaneous leishmaniasis , immunity , cytokine , vaccination , biology , immune system , c57bl/6 , disease , virology , medicine , parasite hosting , world wide web , computer science
Leishmaniasis is a parasitic disease affecting ∼12 million people. Control of infection (e.g. in C57BL/6 mice) results from IL‐12‐dependent production of IFNγ by Th1/Tc1 cells. In contrast, BALB/c mice succumb to infection because of preferential Th2‐type cytokine induction. Infected dendritic cells (DC) represent important sources of IL‐12. Genetically determined differences in DC IL‐1α/β production contribute to disease outcome. Whereas the course of disease was not dramatically altered in IL‐1RI −/− mice, local administration of IL‐1α to infected C57BL/6 mice improved disease outcome. To definitively elucidate the involvement of IL‐1 in immunity against leishmaniasis, we now utilized IL‐1α/β‐double‐deficient C57BL/6 mice. C57BL/6 mice are believed to be a good surrogate model for human, self limited cutaneous leishmaniasis (CL). Leishmania major ‐infected IL‐1α/β −/− mice were resistant to experimental CL comparable to controls. In addition, DC‐based vaccination against leishmaniasis in C57BL/6 mice was independent of IL‐1. Thus, in Leishmania ‐resistant C57BL/6 mice, IL‐1 signalling is dispensable for protection.