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Updated: Aug 11, 2025

A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection
Published on: February 28, 2019
IL-17 Signaling in Keratinocytes Orchestrates the Defense against Staphylococcus aureus Skin Infection
Sonja Moos1, Tommy Regen2, Florian Wanke3
1Department of Dermatology, Heidelberg University Hospital, Heidelberg, Germany; Institute for Molecular Medicine, Paul Klein Center for Immune Intervention, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Keratinocytes (KCs) lacking IL-17RA signaling disrupt skin microbiota, leading to T17 cell expansion and increased Staphylococcus aureus susceptibility. KCs are key in coordinating skin immunity against pathogens.
Area of Science:
- Immunology
- Microbiology
- Dermatology
Background:
- Keratinocytes (KCs) form the skin barrier, crucial for pathogen defense.
- Interleukin-17 (IL-17) signaling is vital for skin immunity.
- IL-17RA deficiency in mice leads to Staphylococcus aureus skin infections.
Purpose of the Study:
- To investigate the role of IL-17RA signaling in keratinocytes during Staphylococcus aureus skin infections.
- To elucidate the mechanisms behind T17 cell expansion in IL-17RA-deficient mice.
- To identify the primary target cells of IL-17A and IL-17F in skin immunity.
Main Methods:
- Mice models with targeted IL-17RA deficiency in keratinocytes or T cells.
- Analysis of T17 cell populations (RORγt+ γδ T cells and T helper 17 cells).
- Assessment of skin microbiota composition and susceptibility to S. aureus infection.
Main Results:
- IL-17RA deficiency in KCs, not T cells, caused T17 cell expansion.
- T17 cell expansion was dependent on skin microbiota.
- Mice lacking IL-17RA in KCs exhibited increased S. aureus susceptibility and T17 cell accumulation.
Conclusions:
- Keratinocyte IL-17RA signaling is essential for maintaining skin microbiota homeostasis.
- IL-17RA deficiency on KCs triggers microbiota dysbiosis, leading to T17 cell expansion.
- Keratinocytes are primary targets of IL-17A/F, coordinating skin defense against microbial invaders.
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