Endogenous latent membrane protein 1 in Epstein–Barr virus-infected nasopharyngeal carcinoma cells attracts T lymphocytes through upregulation of multiple chemokines
| Autor: | Shih Yi Wu, Hsiao Ching Lai, Yao Chang, Kenzo Takada, Chien Hsun Lee, Chaio Wei Chen, Ih-Jen Su, Jenn Ren Hsiao |
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| Rok vydání: | 2010 |
| Předmět: |
Herpesvirus 4
Human Chemokine T-Lymphocytes T cell medicine.disease_cause Viral Matrix Proteins Epstein–Barr virus Cell Line Tumor Latent membrane protein 1 Virology Nasopharyngeal carcinoma otorhinolaryngologic diseases medicine Humans Interleukin 8 Chemokine CCL4 Chemokine CCL3 biology Chemotaxis Carcinoma T cell chemotaxis Nasopharyngeal Neoplasms medicine.disease Up-Regulation Chemotaxis Leukocyte stomatognathic diseases medicine.anatomical_structure Gene Expression Regulation Cell culture Immunology Cancer research biology.protein Chemokines |
| Zdroj: | Virology. 405:464-473 |
| ISSN: | 0042-6822 |
| Popis: | Tumor-infiltrating T lymphocytes are considered to facilitate development of Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma (NPC), but how EBV in NPC tumor cells directs T cell infiltration remains unclear. Here we compare EBV-infected NPC cells with and without spontaneous expression of viral latent membrane protein 1 (LMP1) and find that culture supernatants of LMP1-positive NPC cells exert enhanced chemoattraction to primary T cells. Knockdown of endogenous LMP1 in the cells suppresses the chemotactic activity. Endogenous LMP1 in NPC cells upregulates multiple chemokines, among which MIP-1alpha, MIP-1beta and IL-8 contribute to T cell chemotaxis. We further reveal that LMP1-induced production of MIP-1alpha and MIP-1beta in NPC cells requires not only two carboxyl-terminal activation regions of LMP1 but also their downstream NF-kappaB and JNK pathways. This study corroborates that endogenous LMP1 in EBV-infected NPC cells induces multiple chemokines to promote T cell recruitment and perhaps other pathogenic events in NPC. |
| Databáze: | OpenAIRE |
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