Format

Send to

Choose Destination
Indian J Ophthalmol. 2019 Nov;67(11):1821-1828. doi: 10.4103/ijo.IJO_1780_18.

Blockade of IL-27 signaling ameliorates herpes stromal keratitis with upregulated CD4+ Foxp3+ regulatory T cells influx in mice.

Author information

1
Department of Ophthalmology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China.

Abstract

Purpose:

The purpose of this study was to investigate the production of IL-27 p28 and EBI3 in the ocular inflammatory sites, and the role of IL-27 signaling in a model of HSV-1 induced herpetic stromal keratitis (HSK).

Methods:

The BALB/c mice were injected intraperitoneally (24 h before infection) with anti-IL-27 antibody or IgG antibody as control, infected with HSV-1 via corneal scarification, and then injected intraperitoneally with anti-IL-27 antibody or IgG antibody at 1, 3, and 5 days postinfection. Slit lamp and histopathology were used to assess disease outcome. The levels of IL-27 p28 and EBI3 in corneas were determined by western blotting and immunofluorescence. Furthermore, viral titers were determined, and immune cell infiltrates were collected and analyzed by flow cytometry.

Results:

We found that the levels of IL-27 p28 and EBI3 in corneas were elevated significantly at the peak of HSK, and both of them were expressed simultaneously in the epithelium, stroma, and endothelium of corneas. In the group of anti-IL-27 treatment, the severity of the corneal lesion and CD4+ T cells infiltration were significantly decreased, and the percentage of CD4+ Foxp3+ Tregs was upregulated markedly in the spleen, DLNs and cornea of HSK mice compared to IgG treatment.

Conclusion:

These results provided evidence that IL-27 as a pathogenic pro-inflammatory cytokine controlled CD4+ Foxp3+ Tregs production in HSK, which ultimately resulted in promoting the progression of HSK and poor prognosis.

KEYWORDS:

CD4+T cells; Interleukin-27; Tregs; herpes simplex virus type 1; herpetic stromal keratitis

PMID:
31638041
DOI:
10.4103/ijo.IJO_1780_18

Conflict of interest statement

There are no conflicts of interest.

Supplemental Content

Loading ...
Support Center