Pulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells.

ABSTRACT:

Background

Single nucleotide polymorphisms in the human gene for the receptor for advanced glycation end-products (RAGE) are associated with an increased incidence of asthma. RAGE is highly expressed in the lung and has been reported to play a vital role in the pathogenesis of murine models of asthma/allergic airway inflammation (AAI) by promoting expression of the type 2 cytokines IL-5 and IL-13. IL-5 and IL-13 are prominently secreted by group 2 innate lymphoid cells (ILC2s), which are stimulated by the proallergic cytokine IL-33.

Objective

We sought to test the hypothesis that pulmonary RAGE is necessary for allergen-induced ILC2 accumulation in the lung.

Methods

AAI was induced in wild-type and RAGE knockout mice by using IL-33, house dust mite extract, or Alterna

SUBMITTER: Oczypok EA 

PROVIDER: S-EPMC4562894 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature