CD3ε of a pan T cell marker involved in mouse Aspergillus fumigatus keratitis

To explore whether CD3ε is involved in the adaptive immunity of ( ) keratitis in mice and the role of innate and adaptive immunity in it. Mice models of keratitis were established by intra-stromal injection and corneal epithelial scratching. Subconjunctival injections of natamycin, wedelolactone, LO...

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Published inInternational journal of ophthalmology Vol. 17; no. 4; pp. 616 - 624
Main Authors Shi, Wen-Hao, Wang, Li-Mei, Yan, Hai-Jing, Liu, Shi-Long, Yang, Xian, Yang, Xue-Jiao, Che, Cheng-Ye
Format Journal Article
LanguageEnglish
Published China International Journal of Ophthalmology Press 18.04.2024
Press of International Journal of Ophthalmology (IJO PRESS)
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Summary:To explore whether CD3ε is involved in the adaptive immunity of ( ) keratitis in mice and the role of innate and adaptive immunity in it. Mice models of keratitis were established by intra-stromal injection and corneal epithelial scratching. Subconjunctival injections of natamycin, wedelolactone, LOX-1 inhibitor (poly I) or Dectin-1 inhibitor (laminarin) were used to treat mice with keratitis. Mice were pretreated by intraperitoneal injection of anti-mouse CD3ε. We observed the corneal infection of mice under the slit lamp microscope and made a clinical score. The protein expression of CD3ε and interleukin-10 (IL-10) was determined by Western blotting. With the disease progresses, the degree of corneal opacity and edema augmented. In the intra-stromal injection models, CD3ε protein expression began to increase significantly on the 2 day. However, in the scraping epithelial method models, CD3ε only began to increase on the 3 day. After natamycin treatment, the degree of corneal inflammation in mice was significantly attenuated on the 3 day. After wedelolactone treatment, the severity of keratitis worsened. And the amount of CD3ε protein was also reduced, compared with the control group. By inhibiting LOX-1 and Dectin-1, there was no significant difference in CD3ε production compared with the control group. After inhibiting CD3ε, corneal ulcer area and clinical score increased, and IL-10 expression was downregulated. As a pan T cell marker, CD3ε participate in the adaptive immunity of keratitis in mice. In our mice models, the corneas will enter the adaptive immune stage faster. By regulating IL-10, CD3ε exerts anti-inflammatory and repairs effects in the adaptive immune stage.
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Co-first authors: Wen-Hao Shi, Li-Mei Wang, and Hai-Jing Yan
ISSN:2222-3959
2227-4898
DOI:10.18240/ijo.2024.04.03