Human Retrovirus Infection and Immunodeficiencies. Detection and Significance of Virus-Neutralizing Antibodies

2015 ◽  
pp. 159-166 ◽  
Author(s):  
G. P. Faulkner-Valle ◽  
A. De Rossi ◽  
O. Dalla Gassa ◽  
E. Francavilla ◽  
A. Amadori ◽  
...  
Keyword(s):  
Neutralizing Antibodies ◽  
Retrovirus Infection ◽  
Human Retrovirus

scholarly journals Class Switch Recombination and Somatic Hypermutation of Virus-Neutralizing Antibodies Are Not Essential for Control of Friend Retrovirus Infection

2014 ◽  
Vol 89 (2) ◽  
pp. 1468-1473 ◽  
Author(s):  
Maiko Kato ◽  
Sachiyo Tsuji-Kawahara ◽  
Yuri Kawasaki ◽  
Saori Kinoshita ◽  
Tomomi Chikaishi ◽  
...  
Keyword(s):  
Neutralizing Antibodies ◽  
Somatic Hypermutation ◽  
Cytidine Deaminase ◽  
Class Switch Recombination ◽  
Friend Virus ◽  
Class Switch ◽  
Activation Induced Cytidine Deaminase ◽  
Friend Virus Infection ◽  
Retrovirus Infection ◽  
Deficient Mice

Toll-like receptor 7 and Myd88 are required for antiretroviral antibody and germinal center responses, but whether somatic hypermutation and class-switch recombination are required for antiretroviral immunity has not been examined. Mice deficient in activation-induced cytidine deaminase (AID) resisted Friend virus infection, produced virus-neutralizing antibodies, and controlled viremia. Passive transfer demonstrated that immune IgM from AID-deficient mice contributes to Friend virus control in the presence of virus-specific CD4+T cells.

Cellular and viral protein interactions regulating IκBα activity during human retrovirus infection

1997 ◽  
Vol 62 (1) ◽  
pp. 82-92 ◽  
Author(s):  
John Hiscott ◽  
Pierre Beauparlant ◽  
Pascale Crepieux ◽  
Carmela DeLuca ◽  
Hakju Kwon ◽  
...  
Keyword(s):  
Protein Interactions ◽  
Viral Protein ◽  
Retrovirus Infection ◽  
Human Retrovirus

Endothelial Cell Protein S Synthesis Is Upregulated by the Complex of IL-6 and Soluble IL-6 Receptor

1997 ◽  
Vol 77 (05) ◽  
pp. 1014-1019 ◽  
Author(s):  
W Craig Hooper ◽  
Donald J Phillips ◽  
Bruce L Evatt
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Line ◽  
Neutralizing Antibodies ◽  
Hepatoma Cell ◽  
Protein S ◽  
Oncostatin M ◽  
Cell Protein ◽  
Microvascular Endothelial Cell ◽  
Hepatoma Cell Line

SummaryWe have recently demonstrated that the proinflammatory cytokine, interleukin-6 (IL-6), could upregulate the production of protein S in the human hepatoma cell line, HepG-2, but not in endothelial cells. In this study, we have demonstrated that the combination of exogenous IL-6 and soluble IL-6 receptor (sIL-6R) could significantly upregulate protein S production in both primary human umbilical vein endothelial cells (HUVEC) and in the immortalized human microvascular endothelial cell line, HMEC-1. The IL-6/sIL-6R complex was also able to rapidly induce tyrosine phosphorylation of the IL-6 transducer, gpl30. Neutralizing antibodies directed against either IL-6 or gpl30 blocked protein S upregulation by the IL-6/sIL-6R complex. It was also observed that exogenous sIL-6R could also upregulate protein S by forming a complex with IL-6 constitutively produced by the endothelial cell. Two other cytokines which also utilize the gpl30 receptor, oncostatin M (OSM) and leukemia inhibitory factor (LIF), were also able to upregulate endothelial cell protein S. This study demonstrates a mechanism that allows endothelial cells to respond to IL-6 and also illustrates the potential importance of circulating soluble receptors in the regulation of the anticoagulation pathway.

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