Increased airway smooth muscle (ASM) contractility and the development of airway hyperresponsiveness (AHR) are cardinal features of asthma, but the signaling pathways that promote these changes are poorly understood. Tyrosine phosphorylation is tightly regulated by the opposing actions of protein tyrosine kinases and phosphatases, but little is known about whether tyrosine phosphatases influence AHR. Here, we demonstrate that genetic inactivation of receptor-like protein tyrosine phosphatase J (
Tamiko R. Katsumoto, Makoto Kudo, Chun Chen, Aparna Sundaram, Elliott C. Callahan, Jing W. Zhu, Joseph Lin, Connor E. Rosen, Boryana N. Manz, Jae W. Lee, Michael A. Matthay, Xiaozhu Huang, Dean Sheppard, Arthur Weiss
CD148-deficient mice are protected from HDM-induced AHR with minimal attenuation of inflammatory response to allergen.