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Immunosuppressive HLA-G molecule is upregulated in alveolar epithelial cells after influenza A virus infection

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Le Bouder, Fanny | Khoufache, Khaled | Menier, Catherine | Mandouri, Yassmina | Keffous, Mahmoud | Lejal, Nathalie | Krawice-Radanne, Irène | Carosella, Edgardo D. | Rouas-Freiss, Nathalie | Riteau, Beatrice

Edité par CCSD ; Elsevier -

International audience. Influenza virus type A (IAV) infections constitute an important economic burden and raise health-care problems. Host defense mechanisms usually clear IAV infections after a few days by exploiting a variety of cellular immune responses. However, increasing the production of immunosubversive molecules is a mechanism by which viruses escape host surveillance. In this regard, the nonclassical HLA class I molecule HLA-G displays strong tolerogenic properties.Weshow here that several strains of IAV differently upregulate HLA-G expression, at both the mRNA and protein levels, in alveolar epithelial cells. Thus the virulence of IAV may be caused by the capability of different strains to upregulate HLA-G allowing their escape from host immune responses.

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