E-viri
Recenzirano
Odprti dostop
-
Segawa, S; Goto, D; Iizuka, A; Kaneko, S; Yokosawa, M; Kondo, Y; Matsumoto, I; Sumida, T
Clinical and experimental immunology, 09/2016, Letnik: 185, Številka: 3Journal Article
Summary Interstitial pneumonia (IP) is a chronic progressive interstitial lung disease associated with poor prognosis and high mortality. However, the pathogenesis of IP remains to be elucidated. The aim of this study was to clarify the role of pulmonary gammadeltaT cells in IP. In wild-type (WT) mice exposed to bleomycin, pulmonary gammadeltaT cells were expanded and produced large amounts of interferon (IFN)-gamma and interleukin (IL)-17A. Histological and biochemical analyses showed that bleomycin-induced IP was more severe in T cell receptor (TCR-delta-deficient (TCRdelta-/-) mice than WT mice. In TCRdelta-/- mice, pulmonary IL-17A+CD4+ Τ cells expanded at days 7 and 14 after bleomycin exposure. In TCRdelta-/- mice infused with gammadeltaT cells from WT mice, the number of pulmonary IL-17A+ CD4+ T cells was lower than in TCRdelta-/- mice. The examination of IL-17A-/- TCRdelta-/- mice indicated that gammadeltaT cells suppressed pulmonary fibrosis through the suppression of IL-17A+CD4+ T cells. The differentiation of T helper (Th)17 cells was determined in vitro, and CD4+ cells isolated from TCRdelta-/- mice showed normal differentiation of Th17 cells compared with WT mice. Th17 cell differentiation was suppressed in the presence of IFN-gamma producing gammadeltaT cells in vitro. Pulmonary fibrosis was attenuated by IFN-gamma-producing gammadeltaT cells through the suppression of pulmonary IL-17A+CD4+ T cells. These results suggested that pulmonary gammadeltaT cells seem to play a regulatory role in the development of bleomycin-induced IP mouse model via the suppression of IL-17A production.
Avtor
Vnos na polico
Trajna povezava
- URL:
Faktor vpliva
Dostop do baze podatkov JCR je dovoljen samo uporabnikom iz Slovenije. Vaš trenutni IP-naslov ni na seznamu dovoljenih za dostop, zato je potrebna avtentikacija z ustreznim računom AAI.
Leto | Faktor vpliva | Izdaja | Kategorija | Razvrstitev | ||||
---|---|---|---|---|---|---|---|---|
JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
Baze podatkov, v katerih je revija indeksirana
Ime baze podatkov | Področje | Leto |
---|
Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
---|
Vir: Osebne bibliografije
in: SICRIS
To gradivo vam je dostopno v celotnem besedilu. Če kljub temu želite naročiti gradivo, kliknite gumb Nadaljuj.