OBJECTIVES:

miR-155 has been associated with both innate and adaptive immune responses. SOCS1, which is involved in Treg survival and function, is a direct target of miR-155 in Treg.Since there are two subsets of Treg (nTreg and iTreg), we therefore investigated miR-155 expression in these cells and their possible impact on Treg function after knocking down.

METHODS:

Expression of miR-155 was assessed in UCB nTreg, iTreg and control CD4+CD25- T cells by RT-PCR. Then miR-155 was knocked down by antagomir. Phenotypes and cytokines were assayed by flow cytometry. Interference with biological activity of miR-155 was evaluated in functional Treg assays.

RESULTS:

Besides cytokine differences, nTreg showed significantly lower miR-155 expression and higher SOCS1 expression compared to iTreg. After knock-down of miR-155, SOCS1 expression was the only target we found increased strongly in iTreg while nTreg was not affected. SOCS1 related cytokines were reduced in iTreg after knock-down of miR-155. Diminution of miR-155 expression increased the function of iTreg in the CFSE assay.

CONCLUSIONS:

Our results demonstrate that miR-155–SOCS1 signaling pathway is different between UCB iTreg and nTreg. Knock-down of miR-155 facilitates SOCS1 expression in iTreg. And increased SOCS1 expression is the main reason that iTreg acquires better suppressive function after knock-down of miR-155.

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