In:
The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 125.9-125.9
Abstract:
Immunotherapy (IT) is one of the most effective therapies for increasing allergic diseases worldwide including allergic asthma. Previously, we have established a murine model of subcutaneous IT for experimental allergic asthma. We demonstrated that main components of allergic asthma induced by T-bet deficiency such as airway hyperresponsiveness could be ameliorated. These data suggested that the molecular mechanism induced by IT is T-bet independent. To analyze this yet unknown mechanism we started to investigate IL-6 expression in this model. IL-6 is a cytokine produced by several cell types of the innate as well as adaptive immune system. We previously described that IL-6 is increased in the lung cells of T-bet deficient (T-bet-/-) naïve mice as compared to wild type littermates. In a murine model of allergic asthma we found that IL-6 is significantly down-regulated in the lung of T-bet-/- mice that have been treated according to the IT protocol. Likewise, we found that the newly discovered cytokine IL-33, of the IL-1 family, is significantly up-regulated in the lung of T-bet-/- mice in experimental asthma and down-regulated after IT. In conclusion we discovered that the protective mechanism of the IT comprises down-regulation of IL-6 and IL-33. These findings could be considered for future novel therapy for allergic asthma.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.188.Supp.125.9
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2012
detail.hit.zdb_id:
1475085-5
