Notably, genetic interaction between <i>RhoA</i> and <i>SHP2</i> indicated that RhoA inactivation and <i>SHP2</i> deletion synergistically attenuated the allergen-induced eosinophil infiltration into lungs and airway hyperreactivity, whereas overexpression of active RhoA robustly restored the <i>SHP2</i> deletion-resultant attenuation of allergen-induced eosinophil recruitment into lungs and airway hyperreactivity as well.
The analysis of pairwise gametic type distribution for ACP1, ADA and MN polymorphisms has shown that the pattern of differences between bronchial asthma and controls is opposite to that observed between CD and controls.