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IL ‐17A/F in Leishmania major ‐resistant C57 BL /6 mice
Author(s) -
DietzeSchwonberg Kirsten,
Lopez Kostka Susanna,
Lorenz Beate,
Regen Tommy,
Waisman Ari,
von Stebut Esther
Publication year - 2019
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/exd.13896
Subject(s) - leishmania major , phenotype , interleukin 17 , proinflammatory cytokine , immunology , biology , leishmania , chemokine , secretion , leishmaniasis , disease , lesion , inflammation , medicine , parasite hosting , genetics , pathology , endocrinology , gene , world wide web , computer science
Proinflammatory IL ‐17 plays an important role in various diseases and defence 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 C57 BL /6 mice worsened disease outcome. Since C57 BL /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 C57 BL /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.