Cutaneous allergen sensitization is critical for allergic humoral responses controlled by IL-13 receptor-expressing conventional dendritic cells

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Abstract Skin barrier dysfunction in the setting of atopic dermatitis (AD) leads to cutaneous allergen sensitization (CAS).1 The atopic march hypothesis proposes that CAS leads to the subsequent development of other allergic disorders such as asthma and food allergy.2-5 The latter is associated with IgE-mediated anaphylaxis6. However, the precise mechanisms by which CAS promotes IgE-mediated allergic responses remain unclear. We thus established a CAS model of anaphylaxis and identified a unique role of the Interleukin (IL)-13 signal in DCs to generate anaphylactic IgE responses. Single-cell RNA-seq revealed the emergence of IL-13 receptor alpha 1 chain (IL-13Rα1)-expressing type 2 conventional dendritic cells (cDC2s) in CAS. Similar DC populations were identified in allergic rhinitis humans with cedar pollan-specific IgE antibodies. Lineage-specific disruption of IL-13 signaling resulted in a marked reduction in cDC2s that highly expressed MHC class II: these cells controlled the germinal center entry of TFH cells required for IgE responses. These data reveal a unique role for IL-13 in controlling the expansion of MHCIIhi cDC2s and associated TFH cell responses in the setting of allergy.

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