MiR-669b-3p regulates CD4+ T cell function by down-regulating indoleamine-2, 3-dioxygenase.

Abstract:

OBJECTIVE:Acute rejection is a major cause of morbidity and mortality after solid organ transplantation. Therefore, optimizing treatment strategies and improving curative effect is urgent and necessary. Reliable biomarkers for acute rejection and the underlying molecular mechanisms remain to be determined. METHODS:In this study, we established a mouse-to-mouse cardiac transplantation model and identified miR-669b-3p as a potential biomarker of acute rejection using a microRNA polymerase chain reaction (PCR)-based chip assay. RESULTS:Further analyses showed that miR-669b-3p negatively regulated indoleamine-2,3-dioxygenase (IDO), a rate-limiting enzyme of tryptophan catabolism inhibiting T cell function. Using mixed lymphocyte reaction assay, we showed that miR-669b-3p increased proliferation stimulation index and inhibited apoptosis in CD4+ T cells. Moreover, miR-669b-3p regulated the expression of inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and Interleukin 10 (IL-10) and contributed to cytokine shift towards a Th2-dominant response. CONCLUSION:Our results advance the current understanding of the immune regulatory function of miRNA and shed light on the role of miR-669b-3p in CD4+ T cells, suggesting that miR-669b-3p is a potential target for acute allograft rejection.

journal_name

Transpl Immunol

journal_title

Transplant immunology

authors

Li C,Wang X,Yuan F,Zhao Z,Zhang B,Zhang J,Li W,Liu T

doi

10.1016/j.trim.2020.101320

subject

Has Abstract

pub_date

2020-10-01 00:00:00

pages

101320

eissn

0966-3274

issn

1878-5492

pii

S0966-3274(20)30111-8

journal_volume

62

pub_type

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