Purpose: Little data is currently available on the use of the impulse oscillometry system (IOS) parameter in analyzing the lung function of young children with cough-variant asthma (CVA) and classic asthma. The aims of this study were to evaluate the bronchial responsiveness between patients with CVA and those with classic asthma using dose-response slope and various cutoff values. Methods: A methacholine challenge test and a pulmonary function test were performed in 43 children with classic asthma and 26 children with CVA using IOS, and the respiratory resistance (Rrs) and reactance (Xrs) were obtained. The bronchial responsiveness were assessed by provocative concentration causing an 80% fall from baseline in reactance at 5 Hz (PC80_Xrs5) and a 40% increase in resistance at 5 Hz (PC40_Rrs5) and calculating from the degree of dose-response slope (DRS) for airway resistance and reactance. Results: There was no significant difference in base lung function between the two groups. However, the mean DRS_Xrs5 and the number who showed more than an 80% fall in reactance were significantly higher in classic asthma group than those in CVA group (P= 0.040 and P= 0.040, respectively). Conclusion: The use of DRS in oscillatory reactance at 5 Hz is useful for the differential diagnosis of classic asthma and CVA based on bronchial hyperresponsiveness. (Allergy Asthma Respir Dis 2013;1:309-313) Allergy Asthma Respir Dis 1(4):309-313, December 2013 http://dx.

Abbreviations: CaN, calcineurin; CsA, cyclosporin A; HVEM, herpesvirus entry mediator; LIGHT, l ymphotoxin homolog, which exhibits inducible expression and competes with HSV g lycoprotein D for HveA and is expressed on T-lymphocytes; NFAT, nuclear factor of activated T cells; TNFR, tumor necrosis factor receptor; TR2, TNFR-related 2 AbstractTumor necrosis factor receptor-related 2 (TR2, HVEM or TNFRSF-14) plays an important role in immune responses, however, the mechanisms regulating its expression are unclear. To understand the control of TR2 gene expression, we studied the upstream region of the gene. Gel supershift assays revealed inducible binding of nuclear factor of activated T cells (NFAT) to a putative NFAT site within the TR2 promoter. Furthermore, cotransfection of a dominant negative NFAT construct, or siRNA for NFAT, resulted in increased expression of a TR2 reporter gene. Our findings demonstrate that NFAT negatively regulates TR2 expression in activated T cells.