{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T18:11:36Z","timestamp":1792174296781,"version":"4.4.0"},"reference-count":40,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,5,2]],"date-time":"2023-05-02T00:00:00Z","timestamp":1682985600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004431","name":"Fondation de France","doi-asserted-by":"publisher","award":["120246, 89967"],"award-info":[{"award-number":["120246, 89967"]}],"id":[{"id":"10.13039\/501100004431","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003768","name":"Universit\u00e9 de Strasbourg","doi-asserted-by":"publisher","award":["NA"],"award-info":[{"award-number":["NA"]}],"id":[{"id":"10.13039\/501100003768","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec><jats:title>Introduction<\/jats:title><jats:p>The particularities of the ocular immune environment and its barrier protection in the context of infection are not well elucidated. The apicomplexan parasite <jats:italic>Toxoplasma gondii<\/jats:italic> is one of the pathogens successfully crossing this barrier and establishing chronic infection in retinal cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>As a first approach, we studied the initial cytokine network in vitro in four human cell lines: Retinal pigmented epithelial (RPE), microglial, astrocytic and M\u00fcller cells. Furthermore, we looked at the consequences of retinal infection on the integrity of the outer blood-retina barrier (oBRB). We particularly focused on the roles of type I and type III interferons, (IFN-\u03b2 and IFN-\u03bb). Especially IFN-\u03bb is known for its significant role in barrier defense. However, its effect on the retinal barrier or <jats:italic>T. gondii<\/jats:italic> infection remains unexplored, unlike IFN-\u03b3, which has been extensively studied in this context.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results and Discussion<\/jats:title><jats:p>Here, we show that stimulation with type I and III interferons did not limit parasite proliferation in retinal cells we tested. However, IFN-\u03b2 and IFN-\u03b3 strongly induced inflammatory or cell-attracting cytokine production, whereas IFN-\u03bb1 showed less inflammatory activity. Concomitant <jats:italic>T. gondii<\/jats:italic> infection influenced these cytokine patterns, distinctly depending on the parasite strain. Interestingly, all these cells could be stimulated to produce IFN-\u03bb1. Using an in vitro oBRB model based on RPE cells, we observed that interferon stimulation strengthened membrane localization of the tight junction protein ZO-1 and enhanced their barrier function, in a STAT1-independent manner.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Together, our model shows how <jats:italic>T. gondii<\/jats:italic> infection shapes the retinal cytokine network and barrier function, and demonstrates the role of type I and type III interferons in these processes.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fimmu.2023.1148037","type":"journal-article","created":{"date-parts":[[2023,5,2]],"date-time":"2023-05-02T20:41:39Z","timestamp":1683060099000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":11,"title":["Type I and III interferons shape the retinal cytokine network and barrier function in an in vitro model of ocular 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