Protective role of NFATc2 in CD8+ long lived memory T cells in an allergy model : P234
Details
Serval ID
serval:BIB_B8C7B61549EC
Type
Inproceedings: an article in a conference proceedings.
Publication sub-type
Poster: Summary – with images – on one page of the results of a researche project. The summaries of the poster must be entered in "Abstract" and not "Poster".
Collection
Publications
Institution
Title
Protective role of NFATc2 in CD8+ long lived memory T cells in an allergy model : P234
Title of the conference
Abstracts of the Joint Annual Meeting of Immunology of the Austrian and German Societies (ÖGAI, DGfI)
Address
Vienna, September 3-6, 2008
ISBN
0043-5325
Publication state
Published
Issued date
2008
Peer-reviewed
Oui
Volume
120
Series
Wiener Klinische Wochenschrift
Pages
130-131
Language
english
Notes
The development of allergic immune responses is mediated by CD4+ effector T cells producing T helper 2 (Th2) cytokines as well as by CD8+ T cells that predominate over cytokines such as interferon-gamma (IFN-γ). However the role of IFN-γ in asthma is not fully understood. We demonstrate that mice
lacking nuclear factor of activated T cells-2 (NFATc2) developed increased airway hyperresponsiveness (AHR) and had increased serum IgE levels in the absence of exogenous allergen challenge. This AHR is associated with increased Th2 CD4+ T cell as well as CD8+ T cells defective in interferongamma (IFN-γ) and IL-2 production. Moreover, lung CD8+ T
cells from NFATc2 (-/-) mice contained increased numbers of CD8+ CD122+ CD127+ long lived memory T cells releasing increased amounts of interleukin-10 (IL-10). Adoptive transfer of ovalbumin (OVA) specific NFATc2 (-/-) CD8+ and NFATc2 (-/-) CD4+ T cells enhanced AHR and IL-17 levels while reducing IFN-γ in the airways of SCID reconstituted mice as compared
to those adoptively transferred with NFATc2(+/+)CD8+ and NFATc2 (-/-) CD4+ T cells . Interestingly, depletion of CD8+CD122+ T cells abrogated the increased AHR, eosinophils, and increased IFN-gamma observed in the BALF
of CD4+ NFATc2 (-/-) /CD8+ NFATc2 (-/-) T cell-reconstituted SCID mice. In conclusion NFATc2 expression in long lived memory CD8+ T cells controls directly the IFN-γ and IL-2 expression in CD8+ T cell, which then limits Th17 and Th2 development in the airways in this allergy model.
lacking nuclear factor of activated T cells-2 (NFATc2) developed increased airway hyperresponsiveness (AHR) and had increased serum IgE levels in the absence of exogenous allergen challenge. This AHR is associated with increased Th2 CD4+ T cell as well as CD8+ T cells defective in interferongamma (IFN-γ) and IL-2 production. Moreover, lung CD8+ T
cells from NFATc2 (-/-) mice contained increased numbers of CD8+ CD122+ CD127+ long lived memory T cells releasing increased amounts of interleukin-10 (IL-10). Adoptive transfer of ovalbumin (OVA) specific NFATc2 (-/-) CD8+ and NFATc2 (-/-) CD4+ T cells enhanced AHR and IL-17 levels while reducing IFN-γ in the airways of SCID reconstituted mice as compared
to those adoptively transferred with NFATc2(+/+)CD8+ and NFATc2 (-/-) CD4+ T cells . Interestingly, depletion of CD8+CD122+ T cells abrogated the increased AHR, eosinophils, and increased IFN-gamma observed in the BALF
of CD4+ NFATc2 (-/-) /CD8+ NFATc2 (-/-) T cell-reconstituted SCID mice. In conclusion NFATc2 expression in long lived memory CD8+ T cells controls directly the IFN-γ and IL-2 expression in CD8+ T cell, which then limits Th17 and Th2 development in the airways in this allergy model.
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Create date
15/10/2009 8:43
Last modification date
20/08/2019 16:26