Elevated blood levels of soluble tumor necrosis factor receptors in nasopharyngeal carcinoma: correlation with humoral immune response to lytic replication of Epstein-Barr virus

Citation
P. Feng et al., Elevated blood levels of soluble tumor necrosis factor receptors in nasopharyngeal carcinoma: correlation with humoral immune response to lytic replication of Epstein-Barr virus, INT J ONCOL, 15(1), 1999, pp. 167-172
Citations number
33
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
INTERNATIONAL JOURNAL OF ONCOLOGY
ISSN journal
10196439 → ACNP
Volume
15
Issue
1
Year of publication
1999
Pages
167 - 172
Database
ISI
SICI code
1019-6439(199907)15:1<167:EBLOST>2.0.ZU;2-S
Abstract
Nasopharyngeal carcinoma (NPC) is tightly associated with Epstein-Barr viru s (EBV) infection and a heavy infiltration of lymphoid cells in the tumor t issue. Although various lines of evidence have shown that the immune system s of NPC patients have the potential to attack the tumor cells, it is not y et understood how this potential is blocked. In this study we determined th e circulatory soluble tumor necrosis factor receptors (sTNFRI and sTNFRII), which are proven to be inhibitory to the anti-tumor effects of tumor necro sis factor-alpha (TNF-alpha), in NPC patients. The serum concentration of b oth sTNFRI and sTNFRII was determined with an ELISA method, and shown to be significantly higher in 28 NPC patients than in matched healthy controls. This elevation was found to be positively correlated with the serum titers of IgA against EBV early antigens and viral capsid antigens in NPC patients , suggesting that the increased serum concentration of sTNFRI and sTNFRII i s possibly due to the EBV infection in NPC tumor cells, This is partly supp orted by FAGS analysis of the circulatory T cells. Phenotypical expression of activation markers such as CD25, CD38, CD69 and CD71 in blood T cells wa s not significantly different between the NPC and control individuals, indi cating the elevation of the sTNFRs is indeed derived from the local immune response in the tumor area. Based on these results, it seems that the incre ased sTNFRs may act as an inhibitor to decrease the host immune response to wards tumor cells in NPC patients.