Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity.

ABSTRACT:

Background

Asthma has been considered an immunologic disease mediated by T(H)2 cells and adaptive immunity. However, clinical and experimental observations suggest that additional pathways might regulate asthma, particularly in its nonallergic forms, such as asthma associated with air pollution, stress, obesity, and infection.

Objectives

Our goal was to understand T(H)2 cell-independent conditions that might lead to airway hyperreactivity (AHR), a cardinal feature of asthma.

Methods

We examined a murine model of experimental asthma in which AHR was induced with glycolipid antigens, which activate natural killer T (NKT) cells.

Results

In this model AHR developed rapidly when mice were treated with NKT cell-activating glycolipid antigens, even in the absence of c

SUBMITTER: Kim HY 

PROVIDER: S-EPMC3246069 | biostudies-literature | 2012 Jan

REPOSITORIES: biostudies-literature