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B7-H1, which represses EBV-immortalized B cell killing by autologous T and NK cells, is oppositely regulated by c-Myc and EBV latency III program at both mRNA and secretory lysosome levels.
Durand-Panteix, Stéphanie; Farhat, Mona; Youlyouz-Marfak, Ibtissam; Rouaud, Pauline; Ouk-Martin, Catherine; David, Amandine; Faumont, Nathalie; Feuillard, Jean; Jayat-Vignoles, Chantal.
Afiliación
  • Durand-Panteix S; Centre National de la Recherche Scientifique, Unité Mixte de Recherche CNRS 7276, Faculté de Médecine, 87025 Limoges Cedex, France.
J Immunol ; 189(1): 181-90, 2012 Jul 01.
Article en En | MEDLINE | ID: mdl-22661084
EBV-immortalized B cells induce a complex immune response such that the virus persists as a clinically silent infection for the lifetime of the infected host. B7-H1, also called PD-L1, is a cosignaling molecule of the B7 family that can inhibit activated T cell effectors by interaction with its receptor PD-1. In this work, we have studied the dependence of B7-H1 on NF-κB and c-Myc, the two main transcription factors in EBV latency III proliferating B cells, on various lymphoblastoid and Burkitt lymphoma cell lines, some of them being inducible or not for the EBV latency III program and/or for c-Myc. We found that B7-H1 repressed killing of EBV-immortalized B cells by their autologous T and NK cells. At the mRNA level, NF-κB was a weak inducer whereas c-Myc was a strong repressor of B7-H1 expression, an effect mediated by STAT1 inhibition. At the protein level, B7-H1 molecules were stored in both degradative and unconventional secretory lysosomes. Surface membrane B7-H1 molecules were constitutively internalized and proteolyzed in lysosomes. The EBV latency III program increased the amounts of B7-H1-containing secretory lysosomes and their export to the surface membrane. By repressing actin polymerization, c-Myc blocked secretory lysosome migration and B7-H1 surface membrane export. In addition to B7-H1, various immunoregulatory molecules participating in the immunological synapse are stored in secretory lysosomes. By playing on actin polymerization, c-Myc could thus globally regulate the immunogenicity of transformed B cells, acting on export of secretory lysosomes to plasma membrane.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: ARN Viral / Células Asesinas Naturales / Subgrupos de Linfocitos B / Subgrupos de Linfocitos T / Proteínas Proto-Oncogénicas c-myc / Latencia del Virus / Herpesvirus Humano 4 / Antígeno B7-H1 / Lisosomas Límite: Humans Idioma: En Revista: J Immunol Año: 2012 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: ARN Viral / Células Asesinas Naturales / Subgrupos de Linfocitos B / Subgrupos de Linfocitos T / Proteínas Proto-Oncogénicas c-myc / Latencia del Virus / Herpesvirus Humano 4 / Antígeno B7-H1 / Lisosomas Límite: Humans Idioma: En Revista: J Immunol Año: 2012 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos