New Perspectives on Classical Alarmin Responses to Intestinal Helminth Infection

Interleukins 33, 25, and thymic stromal lymphopoietin (TSLP) are core components of type two immune responses and have been studied extensively using helminth infection models. However, many questions remain regarding their cellular sources, their immune recipients, as well as how they shape immunity. Recent literature has demonstrated non-epithelial alarmin production, acting primarily on lymphoid effector cells, and has suggested a role for alarmins in licensing of effector function in tissues during immunity, in dissent with conceptions of classical alarmins as epithelium-derived, myeloid-targeting, and induced prior to adaptive responses. This review examines recent findings in alarmin helminth interactions at barrier sites and discusses the wider implications for how alarmin responses are conceptualised.