当前位置： SCI文献检索 > INTERNATIONAL IMMUNOPHARMACOLOGY期刊下所有文献 > Dendritic cells transfected with indoleamine 2,3-dioxygenase gene suppressed acute rejection of cardiac allograft.

Dendritic cells transfected with indoleamine 2,3-dioxygenase gene suppressed acute rejection of cardiac allograft.

Abstract：

BACKGROUND:Immunomodulation by indoleamine 2,3-dioxygenase (IDO) has been documented in many studies yet its underlying mechanisms remain undefined, especially in solid organ transplantation. Recent research demonstrated that the active expression of IDO in dendritic cells (DCs) regulates immune reaction. This study assessed whether DCs transfected with IDO gene inhibit T cells responses and suppress cardiac allograft rejection. METHODS:Adenovirus vector containing IDO gene was transfected into DCs to obtain IDO-positive DCs (IDO(+) DCs). To evaluate the effect of IDO(+) DCs on T cells in vitro, CD4(+) T cell proliferation and apoptosis was assessed in mixed lymphocyte reactions and measured by flow cytometry, respectively. IDO(+) DCs from C57BL/6 mice were injected into BALB/c recipients before heterotopic cardiac transplantation. RESULTS:Supernatant fluids from cultures of IDO(+) DCs had decreased tryptophan and increased kynurenine levels, reflecting IDO activity. IDO(+) DCs suppressed CD4(+) T cell responses in vitro, as reflected by decreased proliferation and increased apoptosis. In the transplant model, IDO(+) DCs prolonged survival and alleviated rejection of cardiac allograft in recipients injected with IDO(+) DCs. In vivo, IDO(+) DCs also significantly impaired CD4(+) T cell responses promoting increased apoptosis and a Th2-dominant cytokine shift. CONCLUSIONS:IDO overexpression in DCs suppressed T cells alloresponses in vitro, and IDO(+) DCs attenuated acute allograft rejection in vivo. Regulation of tryptophan catabolism by means of IDO overexpression in DCs may be a useful approach in cardiac transplantation and immunological tolerance.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Li C,Liu T,Zhao N,Zhu L,Wang P,Dai X

doi

10.1016/j.intimp.2016.03.048

subject

Has Abstract

pub_date

2016-07-01 00:00:00

pages

31-38

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(16)30134-5

journal_volume

36

pub_type

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