title: Inhibition of ERK and proliferation in NK cell lines by soluble HLA-E released from Japanese encephalitis virus infected cells.
abstract: Productive infection of human endothelial cells with Japanese encephalitis virus (JEV), a single stranded RNA virus induces shedding of sHLA-E. We show here that sHLA-E that is released upon infection with this flavivirus can inhibit IL-2 and PMA mediated ERK 1/2 phosphorylation in two NK cell lines, Nishi and NKL. Virus infected or IFN-γ treated cell culture supernatants containing sHLA-E were found to partially inhibit IL-2 mediated induction of CD25 molecules on NKL cells. It was also found that sHLA-E could inhibit IL-2 induced [(3)H]-thymidine incorporation suggesting that, similar to cell surface expressed HLA-E, sHLA-E could also inhibit NK cell responses. Hence JEV-induced shedding of sHLA-E needs further investigation to better understand immune responses in JEV infections since it may have a role in viral evasion of NK cell responses.
authors.affiliation: Department of Biochemistry, Indian Institute of Science, Bangalore 560012, India. Electronic address: fshwetank@hmc.psu.edu.
authors.lastname: Shwetank
authors.affiliation: Department of Biochemistry, Indian Institute of Science, Bangalore 560012, India. Electronic address: date.onkar@gmail.com.
authors.forename: Onkar Sanjay
authors.initials: OS
authors.lastname: Date
authors.affiliation: Department of Experimental and Clinical Medicine "G Salvatore", University of Catanzaro Magna Graecia, Catanzaro 88100, Italy. Electronic address: Ennio.Carbone@ki.se.
authors.forename: Ennio
authors.initials: E
authors.lastname: Carbone
authors.affiliation: Department of Biochemistry, Indian Institute of Science, Bangalore 560012, India. Electronic address: mjnhm@biochem.iisc.ernet.in.
authors.forename: Ramanathapuram
authors.initials: R
authors.lastname: Manjunath
mesh_terms: D002460:Cell Line; D004664:Encephalitis Virus, Japanese / Q000276:immunology*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D015870:Gene Expression; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis* / Q000276:immunology*; D006801:Humans; D007376:Interleukin-2 / Q000378:metabolism / Q000494:pharmacology; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism* / Q000821:virology; D008213:Lymphocyte Activation / Q000276:immunology*; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D000097625:HLA-E Antigens
chemical_list: D048049:Extracellular Signal-Regulated MAP Kinases; D015395:Histocompatibility Antigens Class I; D007376:Interleukin-2; D053645:Interleukin-2 Receptor alpha Subunit; D055654:NK Cell Lectin-Like Receptor Subfamily C; D000097625:HLA-E Antigens
keywords: ERK; Endothelial cells; JEV; NK; Proliferation; sHLA-E