In contrast, S-IgA can also trigger eosinophil degranulation [2,122] through its binding to FcαRI or to a putative C-lectin type SC receptor [123], leading to the release of IL-4 and IL-5, as well as eosinophil peroxidase and eosinophil cationic protein, thereby promoting Th2 inflammation and asthma pathogenesis and exacerbations [124]. This evidence concerns the gene IL4 and asthma.