Haemagglutinin-neuraminidase from HPIV3 mediates human NK regulation of T cell proliferation via NKp44 and NKp46.

Autor: McQuaid S; Viral Immunology Laboratory, School of Nursing and Human Sciences, Dublin City University, Glasnevin, Dublin 9, Ireland.; Present address: Mason Technology Ltd., Dublin, Ireland., Loughran S; Viral Immunology Laboratory, School of Nursing and Human Sciences, Dublin City University, Glasnevin, Dublin 9, Ireland.;  Department of Applied Science, Dundalk Institute of Technology, Co. Louth, Ireland., Power P; Viral Immunology Laboratory, School of Nursing and Human Sciences, Dublin City University, Glasnevin, Dublin 9, Ireland.; Dublin Institute of Technology, Dublin, Ireland., Maguire P; Viral Immunology Laboratory, School of Nursing and Human Sciences, Dublin City University, Glasnevin, Dublin 9, Ireland., Walls D; Molecular Virology Laboratory, School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland., Cusi MG; Department of Molecular Biology, Section of Microbiology, University of Siena, Via Laterina 8, IT - 53100 Siena, Italy., Orvell C; Division of Clinical Virology, F68, Karolinska University Hospital, SE-141 86 Stockholm, Sweden., Johnson P; Viral Immunology Laboratory, School of Nursing and Human Sciences, Dublin City University, Glasnevin, Dublin 9, Ireland.
Jazyk: angličtina
Zdroj: The Journal of general virology [J Gen Virol] 2018 Jun; Vol. 99 (6), pp. 763-767. Date of Electronic Publication: 2018 Apr 23.
DOI: 10.1099/jgv.0.001070
Abstrakt: HPIV3 is a respiratory virus causing airway diseases, including pneumonia, croup, and bronchiolitis, during infancy and childhood. Currently there is no effective vaccine or anti-viral therapy for this virus. Studies have suggested that poor T cell proliferation following HPIV3 infection is responsible for impaired immunological memory associated with this virus. We have previously demonstrated that NK cells mediate regulation of T cell proliferation during HPIV3 infection. Here we add to these studies by demonstrating that the regulation of T cell proliferation during HPIV3 infection is mediated via NK receptors NKp44 and NKp46 and involves the surface glycoprotein haemagglutinin-neuraminidase but not the fusion protein of the virus. These studies extend our knowledge of the regulatory repertoire of NK cells and provide mechanistic insights which may explain reoccurring failures of vaccines against this virus.
Databáze: MEDLINE
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