The PI3K pathway is a potent mediator of several functions associated with asthma pathogenesis, including supporting leukocyte survival, activation, migration andcytokine release. Proper negative regulation of this pathway is integral in order to restrict overactive immune responses. Negative regulation of PI3K is predominantly controlled by the lipid phosphatases PTEN and SHIP-1. Inpp5d (Ship1) deficient mice develop spontaneous airway inflammation and have enhanced sensitivity to allergen induced airway inflammation. We hypothesized that deleting Ship1 expression specifically in lineages known to be crucial for adaptive Th2 responses would uncover more subtle effects that could either positively or negatively regulate disease severity in a mouse model of allergic airway inflammation (AAI).
|Number of pages||1|
|Publication status||Published - 18 Dec 2014|
|Event||Canadian Society of Allergy and Clinical Immunology : Annual Scientific Meeting 2014 - Ottawa, ON, Canada|
Duration: 23 Oct 2014 → 26 Oct 2014
|Other||Canadian Society of Allergy and Clinical Immunology|
|Period||23/10/14 → 26/10/14|