IL-1 signalling is dispensable for protective immunity in Leishmania-resistant mice

Kordula Kautz-Neu, Susanna L. Kostka, Stephanie Dinges, Yoichiro Iwakura, Mark C. Udey, Esther Von Stebut

Research output: Contribution to journalLetterpeer-review

30 Scopus citations


Leishmaniasis is a parasitic disease affecting 12 million people. Control of infection (e.g. in C57BL/6 mice) results from IL12dependent 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.

Original languageEnglish
Pages (from-to)76-78
Number of pages3
JournalExperimental Dermatology
Issue number1
StatePublished - Jan 2011


  • Dendritic cells
  • IL-1
  • L. major


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