Modulation of HLA-G expression in human neural cells after neurotropic viral infections |
| |
Authors: | Lafon Monique Prehaud Christophe Megret Françoise Lafage Mireille Mouillot Gaël Roa Michèle Moreau Philippe Rouas-Freiss Nathalie Carosella Edgardo D |
| |
Institution: | Unité de Neuroimmunologie Virale, Institut Pasteur, 25 rue du Dr Roux, 75724 Paris Cedex 15, France. mlafon@pasteur.fr |
| |
Abstract: | HLA-G is a nonclassical human major histocompatibility complex class I molecule. It may promote tolerance, leading to acceptance of the semiallogeneic fetus and tumor immune escape. We show here that two viruses-herpes simplex virus type 1 (HSV-1), a neuronotropic virus inducing acute infection and neuron latency; and rabies virus (RABV), a neuronotropic virus triggering acute neuron infection-upregulate the neuronal expression of several HLA-G isoforms, including HLA-G1 and HLA-G5, the two main biologically active isoforms. RABV induces mostly HLA-G1, and HSV-1 induces mostly HLA-G3 and HLA-G5. HLA-G expression is upregulated in infected cells and neighboring uninfected cells. Soluble mediators, such as beta interferon (IFN-beta) and IFN-gamma, upregulate HLA-G expression in uninfected cells. The membrane-bound HLA-G1 isoform was detected on the surface of cultured RABV-infected neurons but not on the surface of HSV-1-infected cells. Thus, neuronotropic viruses that escape the host immune response totally (RABV) or partially (HSV-1) regulate HLA-G expression on human neuronal cells differentially. HLA-G may therefore be involved in the escape of certain viruses from the immune response in the nervous system. |
| |
Keywords: | |
本文献已被 PubMed 等数据库收录! |
|