@entity172 Signaling Modulates XXXX and Contributes to Sex Differences in Asthma.

@entity1 @entity32 @entity172 @entity1782 @entity4047 @entity1353 @entity565 @entity566 @entity228 @entity1783 @entity56 @entity7280 @entity288
UNASSIGNED: Asthma is a chronic airway inflammatory disease that affects ~300 million @entity1 worldwide. It is characterized by airway constriction that leads to wheezing, coughing, and @entity1353 . The most common treatments are @entity288 and b2-adrenergic receptor antagonists, which target @entity32 and airway smooth muscle constriction, respectively. The incidence and severity of @entity565 is greater in @entity1 than in @entity1 , and @entity1 are more prone to develop @entity228 -resistant or "hard-to-treat" @entity565 . Puberty, menstruation, pregnancy, menopause, and @entity7280 are known to contribute to disease outcome in @entity1 , suggesting a role for @entity172 and other hormones impacting @entity32 . Currently, the mechanisms underlying these sex differences are poorly understood, although the effect of sex hormones, such as @entity172 , on @entity32 is gaining interest. Asthma presents as a heterogeneous disease. In typical Th2-type @entity56 , interleukin (IL)-4 and @entity4047 predominate, driving IgE production and recruitment of eosinophils into the lungs. Chronic Th2- @entity32 in the lung results in structural changes and activation of multiple immune cell types, leading to a deterioration of lung function over time. Most immune cells express @entity172 receptors ( @entity1782 , @entity1783 , or the membrane-bound G-protein-coupled ER) to varying degrees and can respond to the hormone. Together these receptors have demonstrated the capacity to regulate a spectrum of immune functions, including adhesion, migration, survival, wound healing, and antibody and cytokine production. This review will cover the current understanding of @entity172 signaling in @entity32 and discuss how this signaling may contribute to sex differences in @entity565 and @entity566 .
