Immunosuppressive HLA-G molecule is upregulated in alveolar epithelial cells after influenza A virus infection.
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. We show 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.
LeBouder
Fanny
F
Unité de Virologie et Immunologie Moléculaires, UR 892 INRA, Domaine de Vilvert, 78352 Jouy-en-Josas, France.
Khoufache
Khaled
K
Menier
Catherine
C
Mandouri
Yassmina
Y
Keffous
Mahmoud
M
Lejal
Nathalie
N
Krawice-Radanne
Irène
I
Carosella
Edgardo D
ED
Rouas-Freiss
Nathalie
N
Riteau
Béatrice
B
D000818:Animals; D002460:Cell Line; D004285:Dogs; D006680:HLA Antigens / Q000032:analysis / Q000096:biosynthesis*; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000032:analysis / Q000096:biosynthesis*; D006801:Humans; D007108:Immune Tolerance; D009980:Influenza A virus / Q000276:immunology*; D007251:Influenza, Human / Q000276:immunology*; D011650:Pulmonary Alveoli / Q000276:immunology* / Q000821:virology; D012333:RNA, Messenger / Q000276:immunology / Q000378:metabolism; D020545:Respiratory Mucosa / Q000276:immunology / Q000821:virology; D015854:Up-Regulation
D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D012333:RNA, Messenger