Literature DB >> 20955202

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.   

Abstract

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.
© 2010 John Wiley & Sons A/S.

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Year:  2010        PMID: 20955202      PMCID: PMC6999702          DOI: 10.1111/j.1600-0625.2010.01172.x

Source DB:  PubMed          Journal:  Exp Dermatol        ISSN: 0906-6705            Impact factor:   3.960


  17 in total

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