Parasite Clearance in Leishmaniasis in Resistant Animals Is Independent of the IL-23/IL-17A Axis

Abstract

E, et al. Bypassing hybridoma technology: HLA-C reactive human single-chain antibody fragments (scFv) derived from a synthetic phage display library (HuCAL) and their potential to discriminate HLA class I specificities. Tissue Antigens 2000;56:1e9. Meister M, Tounsi A, Gaffal E, Bald T, Papatriantafyllou M, Ludwig J, et al. Self-antigen presentation by keratinocytes in the inflamed adult skin modulates T-cell autoreactivity.

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

“…Supernatants were assessed for the amounts of IFNγ and IL‐4 (controls, data not shown), IL‐17A, IL‐17F, IL‐17E and IL‐22 (Figure A). As described before, higher levels of IFNγ and IL‐22 were found in LN cells from C57BL/6 mice, whereas IL‐4 and IL‐17A were predominantly released from BALB/c cells . Interestingly, levels of secreted IL‐17F were comparable from C57BL/6 to BALB/c LN cells.…”

“…[3,7] However, in IL-17A −/− mice on resistant C57BL/6 background disease progression is not altered upon infection with L. major compared to control mice. [8] Nevertheless, artificial overexpression of IL-17A in CD4 + T cells in C57BL/6 mice resulted in worsening of disease. [8] Even though IL-17A and IL-17F share similar receptors, they may not impact the inflammatory process equally, as both cytokines differentially regulate secretion of chemokines.…”

“…Additionally, IL‐17A‐deficient BALB/c mice were protected from progressive disease despite their Th2 phenotype, which was dependent on an absence of the Th17‐mediated recruitment of neutrophils to the lesions . However, in IL‐17A −/− mice on resistant C57BL/6 background disease progression is not altered upon infection with L. major compared to control mice . Nevertheless, artificial overexpression of IL‐17A in CD4 + T cells in C57BL/6 mice resulted in worsening of disease .…”

“…Since C57BL/6 mice lacking only IL-17A exhibited no phenotype, and IL-17A and IL-17F share similar receptors, but differen-| 323 LETTER: MOUSE MUTANTS WITH ABSENT SKIN PHENOTYPE cells. [3,8,13] Interestingly, levels of secreted IL-17F were comparable from C57BL/6 to BALB/c LN cells. We could not detect IL-17E in supernatants of cells isolated from either strain.Next, we determined the source of IL-17A-secreting cells using intracellular FACS staining of draining LN cells.…”

Insufficient generation of Th17 cells in IL‐23p19‐deficient BALB/c mice protects against progressive cutaneous leishmaniasis

“…Both IL-17A −/− and IL-23p19 −/− C57BL/6 mice developed similar lesion volumes, local and systemic parasite burdens and cytokine levels compared to control mice. [6] In contrast, IL-17A levels are highly increased in susceptible BALB/c mice upon infection with L. major, [3] and IL-17A −/− BALB/c mice were protected from progressive disease, [3] indicating that IL-17A plays a critical role for disease outcome in BALB/c mice. In this setting, IL-17A was primarily produced by CD4 + T cells and neutrophils.…”