This theory may explain the observed binding to hTrx here, since it is secreted upon stress16 and possesses distinct properties of a DAMP: we could show that healthy individuals mount a pronounced IFN-γ response accompanied by IL-10 from monocytes, while AD patients with detectable IgE-sensitization against hTrx elicit predominantly IL-13 with reduced IL-10 levels14. This evidence concerns the gene IL13 and Alzheimer disease.