IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice
| Autor: | Esther von Stebut, Mark C. Udey, Klaus G. Griewank, Stephanie Dinges, Susanna Lopez Kostka, Yoichiro Iwakura |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Neutrophils
Immunology Leishmaniasis Cutaneous Biology Interleukin-23 Article Lesion Mice Immune system Th2 Cells Cutaneous leishmaniasis Species Specificity Immunity medicine Immunology and Allergy Animals Leishmania major Genetic Predisposition to Disease Interleukin 4 Cells Cultured Mice Knockout Immunity Cellular Mice Inbred BALB C Interleukin-17 Cell Differentiation Dendritic Cells medicine.disease biology.organism_classification Up-Regulation Mice Inbred C57BL Interleukin 10 Disease Progression Interleukin 17 medicine.symptom |
| Zdroj: | Journal of immunology (Baltimore, Md. : 1950). 182(5) |
| ISSN: | 1550-6606 |
| Popis: | Resistance to leishmaniasis in C57BL/6 mice depends on Th1/Tc1 cells. BALB/c mice preferentially develop Th2 immunity and succumb to infection. We now assessed the role of IL-17 in cutaneous leishmaniasis. During the course of Leishmania major infection, BALB/c CD4 cells and neutrophils produced increased amounts of IL-17 as compared with cells from C57BL/6 mice. This increase was associated with significantly increased IL-23 release from L. major-infected BALB/c dendritic cells (DC), whereas IL-6 and TGF-β1 production by BALB/c and C57BL/6 DC were comparable. Interestingly, lesion sizes in infected IL-17-deficient BALB/c mice were dramatically smaller and failed to progress as compared with those in control mice. Similar amounts of IL-4, IL-10, and IFN-γ were produced by T cells from IL-17-deficient mice and control mice consistent with development of Th2-predominant immunity in all animals. Improved disease outcome was associated with decreased CXCL2-accumulation in lesion sites and decreased neutrophil immigration into lesions of infected IL-17-deficient mice confirming prior observations that enhanced neutrophil recruitment contributes to disease susceptibility in BALB/c mice. This study excludes an important facilitating role for IL-17 in Th1/Th2 development in L. major-infected BALB/c mice, and suggests that IL-23 production by L. major-infected DC maintains IL-17+ cells that influence disease progression via regulation of neutrophil recruitment. |
| Databáze: | OpenAIRE |
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