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1. Keratinocyte-derived small extracellular vesicles supply antigens for CD1a-resticted T cells and promote their type 2 bias in the context of filaggrin insufficiency

2. Filaggrin insufficiency renders keratinocyte-derived small extracellular vesicles capable of affecting CD1a-mediated T cell responses and promoting allergic inflammation

3. Excess filaggrin in keratinocytes is removed by extracellular vesicles to prevent premature death and this mechanism can be hijacked by Staphylococcus aureus in a TLR2‐dependent fashion

5. Filaggrin insufficiency renders keratinocyte-derived small extracellular vesicles capable of modulating CD1a-mediated T cell responses

7. Excess filaggrin in keratinocytes is removed by extracellular vesicles to prevent premature death and this mechanism can be hijacked by Staphylococcus aureus in a TLR2-dependent fashion

8. Exposure of Keratinocytes to Candida Albicans in the Context of Atopic Milieu Induces Changes in the Surface Glycosylation Pattern of Small Extracellular Vesicles to Enhance Their Propensity to Interact With Inhibitory Siglec Receptors

9. O07 Filaggrin insufficiency renders keratinocyte-derived small extracellular vesicles capable of affecting CD1a-mediated T-cell responses and promoting allergic inflammation.

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