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Augmentation of leukocyte infiltration in murine tumors expressing B-cell derived but not nasopharyngeal carcinoma derived EBV membrane protein LMP1
The Epstein‐Barr virus (EBV) encoded latent membrane protein of B cell origin, B‐LMP1 (B95‐8 prototype) and nasopharyngeal carcinoma (NPC) derived C‐LMP1 (CAO prototype) were transfected individually in S6C adenocarcinoma cells of ACA (H‐2f) origin. We have shown previously that inoculation of B‐LMP...
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Published in: | Journal of medical virology 2000-04, Vol.60 (4), p.417-424 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | The Epstein‐Barr virus (EBV) encoded latent membrane protein of B cell origin, B‐LMP1 (B95‐8 prototype) and nasopharyngeal carcinoma (NPC) derived C‐LMP1 (CAO prototype) were transfected individually in S6C adenocarcinoma cells of ACA (H‐2f) origin. We have shown previously that inoculation of B‐LMP1 expressing S6C cells led to tumor rejection in pre‐immunized, immunocompetent syngeneic ACA mice, whereas the C‐LMP1 transfectants were not immunogenic. Furthermore, B‐LMP1 but not C‐LMP1 expressing S6C cells grew with necrosis and extensive skin damage in non‐immunized mice. A study was carried out to determine whether the in vivo growth pattern of S6C cells expressing two different LMP1 isolates could be correlated to any immunomodulatory mechanism. An increased infiltration of CD45+ leukocytes was found in B‐LMP1 expressing S6C tumors originating in non‐immunized, syngeneic ACA mice. The C‐LMP1 expressors, vector transfectants and untransfected parental tumors had significantly lower number of infiltrating leukocytes. The immunoaccessory molecules ICAM‐1, B7‐1 and MHC Class I and II expression was unaltered in both B‐ and C‐LMP1 transfectants. The data suggest that B‐LMP1 but not C‐LMP1 induce anti‐tumor immune response. J. Med. Virol. 60:417–424, 2000. © 2000 Wiley‐Liss, Inc. |
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ISSN: | 0146-6615 1096-9071 |
DOI: | 10.1002/(SICI)1096-9071(200004)60:4<417::AID-JMV9>3.0.CO;2-O |