Lineage specific role of Ship1 in development of allergic airway inflammation

Matthew J Gold, Michael R Hughes, Frann Antignano, Colby Zaph, Kelly M McNagny

Research output: Contribution to conferenceAbstract

Abstract

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).
Original languageEnglish
Number of pages1
DOIs
Publication statusPublished - 18 Dec 2014
Externally publishedYes
EventCanadian Society of Allergy and Clinical Immunology : Annual Scientific Meeting 2014 - Ottawa, ON, Canada
Duration: 23 Oct 201426 Oct 2014

Other

OtherCanadian Society of Allergy and Clinical Immunology
CountryCanada
CityOttawa, ON
Period23/10/1426/10/14

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