Furthermore, a hypothesis of HSP pathogenesis indicates that infectious agents may induce the secretion of TGF-β in activated T cells, which then increases the serum IgA levels.[20] Some of these IgA molecules binding to endothelial cells induce endothelial cell lysis by indirectly interacting with the complement, or by directly activating endothelial cells to produce IL-8. The gene discussed is CXCL8; the disease is hereditary spastic paraplegia.