4.7 Article

Glucocorticoid treatment inhibits annexin-1 expression in rheumatoid arthritis CD4+ T cells

期刊

RHEUMATOLOGY
卷 47, 期 5, 页码 636-639

出版社

OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/ken062

关键词

annnexin-1; glucocorticoids; T cells; RA

资金

  1. Arthritis Research UK [16125] Funding Source: Medline
  2. Medical Research Council [G0400327, G116/131] Funding Source: Medline
  3. Wellcome Trust [GR040269MA] Funding Source: Medline
  4. MRC [G116/131, G0400327] Funding Source: UKRI
  5. Medical Research Council [G0400327, G9818340B, G116/131] Funding Source: researchfish

向作者/读者索取更多资源

Objective. Annexin-1 (Anx-A1) has been recently shown to play a key role in T-cell activation and to be highly expressed in T cells from RA patients. Here, we investigated the effects of glucocorticoids (GCs) on Anx-A1 expression in T cells in vitro and in vivo. Methods. To evaluate the effects of dexamethasone (Dex) on Anx-A1 expression, human peripheral blood T cells were incubated with Dex and then analysed by real-time PCR and western blotting. Similar experiments were carried out in vivo by measuring Anx-A1 levels in T cells from patients with RA before and after administration of steroids. Results. Incubation of T cells with Dex decreased Anx-A1 levels in a time-dependent fashion and almost abolished its expression after 12 h. Stimulation of T cells pre-incubated with Dex for 12 h with anti-CD3/CD28 led to significant reduction of IL-2 production. Addition of human recombinant Anx-A1 to Dex-treated cells reversed the inhibitory effects of the steroids on anti-CD3/CD28-induced IL-2 production. Treatment of RA patients with steroid decreased Anx-A1 expression in T cells. Conclusions. GCs suppress Anx-A1 expression in T cells in vitro and in vivo. These results provide evidence for a novel pathway by which steroids regulate the adaptive immune response and suggest that Anx-A1 may represent a target for the treatment of autoimmune diseases.

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