tetano
Editor, Senior Moderator
Hum Immunol. 2010 Nov 15. [Epub ahead of print]
Induction of cell surface HLA-G expression in pandemic H1N1 2009 and seasonal H1N1 influenza virus infected patients.
Chen HX, Chen BG, Shi WW, Zhen R, Xu DP, Lin A, Yan WH.
Human Tissue Bank, Taizhou Hospital of Zhejiang Province, Wenzhou Medical College, Linhai, Zhejiang, China; Department of Orthopedics, Taizhou Hospital of Zhejiang Province, Wenzhou Medical College, Linhai, Zhejiang, China.
Abstract
A novel H1N1 virus of swine origin (H1N1v) currently caused a pandemic; however, immunological aspects of the virus infection are limited. HLA-G was speculated play critical roles in viral infection, while its clinical relevance in H1N1 infection remains unknown. In this study, HLA-G expression in peripheral T lymphocytes, monocytes, and CD4+CD25+ FoxP3+ regulatory T (Treg) cells (in 50 H1N1v, 41 seasonal H1N1 infected patients and 27 control subjects) were analyzed with flow cytometry. Plasma soluble HLA-G (sHLA-G, in 28 H1N1v, 29 seasonal H1N1 infected patients and 85 control subjects) were determined with enzyme-linked immunosorbent assay. The percentage of HLA-G-positive T lymphocytes and monocytes among patients with H1N1v and seasonal H1N1 infected was dramatically increased compared to controls (all p<0.001). Treg was markedly increased among H1N1v infected patients compared to normal controls (p=0.041), but not for the seasonal H1N1 infected patients. Meanwhile, no significant difference was observed for sHLA-G levels between the groups. Together, cell surface HLA-G expression was markedly induced in H1N1v and seasonal H1N1 infected patients, and increased Treg was only observed in H1N1v infected patients. Given its immune suppressive property, elevated cell surface HLA-G expression may help the explanation for the virus escaping from host immune responses.
Copyright ? 2010 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
PMID: 21087648 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21087648
Induction of cell surface HLA-G expression in pandemic H1N1 2009 and seasonal H1N1 influenza virus infected patients.
Chen HX, Chen BG, Shi WW, Zhen R, Xu DP, Lin A, Yan WH.
Human Tissue Bank, Taizhou Hospital of Zhejiang Province, Wenzhou Medical College, Linhai, Zhejiang, China; Department of Orthopedics, Taizhou Hospital of Zhejiang Province, Wenzhou Medical College, Linhai, Zhejiang, China.
Abstract
A novel H1N1 virus of swine origin (H1N1v) currently caused a pandemic; however, immunological aspects of the virus infection are limited. HLA-G was speculated play critical roles in viral infection, while its clinical relevance in H1N1 infection remains unknown. In this study, HLA-G expression in peripheral T lymphocytes, monocytes, and CD4+CD25+ FoxP3+ regulatory T (Treg) cells (in 50 H1N1v, 41 seasonal H1N1 infected patients and 27 control subjects) were analyzed with flow cytometry. Plasma soluble HLA-G (sHLA-G, in 28 H1N1v, 29 seasonal H1N1 infected patients and 85 control subjects) were determined with enzyme-linked immunosorbent assay. The percentage of HLA-G-positive T lymphocytes and monocytes among patients with H1N1v and seasonal H1N1 infected was dramatically increased compared to controls (all p<0.001). Treg was markedly increased among H1N1v infected patients compared to normal controls (p=0.041), but not for the seasonal H1N1 infected patients. Meanwhile, no significant difference was observed for sHLA-G levels between the groups. Together, cell surface HLA-G expression was markedly induced in H1N1v and seasonal H1N1 infected patients, and increased Treg was only observed in H1N1v infected patients. Given its immune suppressive property, elevated cell surface HLA-G expression may help the explanation for the virus escaping from host immune responses.
Copyright ? 2010 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
PMID: 21087648 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21087648