In:
International Archives of Allergy and Immunology, S. Karger AG, Vol. 155, No. Suppl. 1 ( 2011), p. 110-116
Abstract:
〈 i 〉 Background: 〈 /i 〉 Glucocorticoid (GC) action on asthma has been partly explained by the inhibition of T cell activation. We analyzed the steroid sensitivity of ovalbumin (OVA) reactive helper T (Th) cell clones both in vitro and in vivo. 〈 i 〉 Method: 〈 /i 〉 For in vitro experiments, Th clones were cultured with antigen-presenting cells, OVA, and various concentrations of dexamethasone (DEX). The proliferative response of each Th clone was measured by 〈 sup 〉 3 〈 /sup 〉 H-thymidine uptake. For in vivo experiments, unprimed BALB/c mice were transferred with Th clones, challenged with OVA, and administered DEX subcutaneously. The number of infiltrating cells in bronchoalveolar lavage fluid (BALF) was measured. 〈 i 〉 Results: 〈 /i 〉 Six Th clones were classified as steroid-sensitive or steroid-resistant clones in terms of the effects of GC on the proliferative responses analyzedin vitro. Airway infiltration of eosinophils and lymphocytes of mice transferred with steroid-sensitive clones were effectively inhibited by the administration of DEX. In contrast, those of mice transferred with steroid-resistant clones were not significantly inhibited by DEX; the number of eosinophils in the BALF of mice transferred with 1 steroid-resistant clone, i.e. T5-1, was only partially reduced. 〈 i 〉 Conclusion: 〈 /i 〉 The steroid sensitivity of Th clones measured in vitro was consistent with that of an adoptively transferred asthma model measuredin vivo. Steroid-sensitive and resistant asthma models seem valuable for understanding the mechanisms of steroid resistance in severe asthma.
Type of Medium:
Online Resource
ISSN:
1018-2438
,
1423-0097
Language:
English
Publisher:
S. Karger AG
Publication Date:
2011
detail.hit.zdb_id:
1482722-0
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