Th2 cells secrete IL-4 and IL-5, which lead to type 1 hypersensitivity.29 The onset of HSP usually follows viral infection, bacterial infection, drug allergy, food allergy, insect bites, or immunization, which implies that allergic reactions may participate in the onset of this disease.5–8 In the presence of IL-4, the majority of B-cells switch immunoglobulin production to produce a vast amount of IgE.30,31 Davin et al12 reported that the incidence of increased plasma IgE levels was significantly higher in patients with HSP and suggested that IgE plays a possible pathogenic role in HSP. Here, IGHE is linked to bacterial infectious disease.