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You are here: Home / Teams / Ohlmann T - REVE / News / Aflatoxin B1 and Epstein-Barr virus-induced CCL22 expression stimulates B cell infection.

Aflatoxin B1 and Epstein-Barr virus-induced CCL22 expression stimulates B cell infection.

Proc Natl Acad Sci U S A. 2024 Apr 16;121(16):e2314426121.doi: 10.1073/pnas.2314426121. Mohamed Ali Maroui, Grace Akinyi Odongo, Lucia Mundo, Francesca Manara, Fabrice Mure, Floriane Fusil, Antonin Jay, Tarik Gheit, Thanos M Michailidis, Domenico Ferrara, Lorenzo Leoncini, Paul Murray, Evelyne Manet, Théophile Ohlmann, Marthe De Boevre, Sarah De Saeger, François-Loïc Cosset, Stefano Lazzi, Rosita Accardi, Zdenko Herceg, Henri Gruffat#, Rita Khoueiry#.

This study provides an insight into the synergistic impact of exposures to environmental agents commonly present in the lymphoma belt regions in Africa such as aflatoxin B1 (AFB1) and oncogenic virus infection, e.g., Epstein–Barr virus (EBV). It reveals mechanisms through which these exposures might contribute to eBL. A focus here is on eBL development in which EBV infection plays a pivotal role together with co-factors such as AFB1 exposure. Our findings have unraveled a role for the AFB1-induced upregulation of the CCL22 in enhancing EBV infection of B cells and therefore a putative role in eBL development. This might corroborate what happens in African sub-Saharan regions where children are first exposed to mycotoxins including AFB1 through food contamination that could deregulate their immune response including CCL22 levels and increase their susceptibility to EBV infection. This would explain in part the high prevalence of eBL in those regions. Moreover, our in vitro and in vivo analyses provide promising evidence for the possible use of CCL22 as a drug target to inhibit eBL development.

Read the paper here: 121(16):e2314426121.doi: 10.1073/pnas.2314426121.

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