IL‐17A/F in Leishmania major‐resistant C57BL/6 mice

Abstract

Proinflammatory IL‐17 plays an important role in various diseases and defense against extracellular microorganisms. Healing of leishmaniasis is promoted by Th1/Tc1 cells, whereas Th2/Treg are associated with worsened disease outcome. In addition, high expression of IL‐17A in Leishmania‐susceptible BALB/c and artificial overexpression of IL‐17A in T cells in resistant C57BL/6 mice worsened disease outcome. Since C57BL/6 mice lacking only IL‐17A exhibited no phenotype, and IL‐17A and IL‐17F share similar receptors, but differentially regulate chemokine secretion, we studied mice lacking both IL‐17A and IL‐17F (IL‐17A/F^‐/‐) in infections with Leishmania major. Interestingly, lesion volumes and parasite burdens were comparable to controls, IL‐17A/F^‐/‐ mice developed a Th1/Tc1 phenotype, and exhibited normal lesion resolution. Thus, in C57BL/6 mice, secretion of IL‐17A and IL‐17F does not influence disease progression. It appears that ‐ depending on the genetic background ‐ cytokines of the IL‐17 family might be responsible for disease progression primarily in susceptible mice.

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