Inception of early-life allergen-induced airway hyperresponsiveness is reliant on IL-13⁺CD4⁺ T cells.

ABSTRACT: Airway hyperresponsiveness (AHR) is a critical feature of wheezing and asthma in children, but the initiating immune mechanisms remain unconfirmed. We demonstrate that both recombinant interleukin-33 (rIL-33) and allergen [house dust mite (HDM) or Alternaria alternata] exposure from day 3 of life resulted in significantly increased pulmonary IL-13⁺CD4⁺ T cells, which were indispensable for the development of AHR. In contrast, adult mice had a predominance of pulmonary Lin^negCD45⁺CD90⁺IL-13⁺ type 2 innate lymphoid cells (ILC2s) after administration of rIL-33. HDM exposure of neonatal IL-33 knockout (KO) mice still resulted in AHR. However, neonatal CD4^creIL-13 KO mice (lacking IL-13⁺CD4⁺

SUBMITTER: Saglani S 

PROVIDER: S-EPMC7613599 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature