title: Differential cytokine expression in EBV positive peripheral T cell lymphomas.
abstract: OBJECTIVE
  To investigate whether specific cytokines are secreted locally at the tumour site in Epstein-Barr virus (EBV) positive peripheral T cell lymphoma (PTCL).
  
  
  METHODS
  An RNase protection assay system was used to study the differential expression of 21 cytokines in parallel in eight cases of EBV positive non-nasal PTCL, and compared with 11 EBV negative non-nasal PTCLs and three EBV positive nasal natural killer (NK) cell lymphomas.
  
  
  RESULTS
  Among the eight EBV positive cases, interferon gamma (IFN-gamma), lymphotoxin beta (LT beta), interleukin 10 (IL-10), tumour necrosis factor alpha (TNF-alpha), transforming growth factor beta 1 (TGF-beta 1), and IL-1 receptor a (IL-Ra) were frequently detectable. IL-15, IL-6, IL-4, IL-1 beta, TNF-beta, and IL-9 were sporadically detectable. Of the frequently detectable cytokines, IFN-gamma and LT beta were commonly detected in the EBV negative cases. For cases with > 50% EBV encoded small non-polyadenylated RNA (EBER) positive cells, IL-10, TNF-alpha, and TGF-beta 1 were detected in three of three cases, and IL-1Ra in two of three cases. For cases with < 20% EBER positive cells, IL-10 was detected in three of five cases, TNF-alpha in two of four cases, but TGF-beta 1 and IL-1Ra were not detected. Interestingly, IL-6 was detected in two of three cases with > 50% EBER positive cells, but only in one of five cases with < 20% EBER positive cells. For comparison, in NK cell lymphomas, IL-10, TNF-alpha, IL-1Ra, and IL-6 were all detectable, but TGF-beta 1 was not detected at all. Immunohistochemical staining revealed IL-10 in many cells; in contrast, EBV latent membrane protein 1 (LMP1) was only found to be positive in isolated cells.
  
  
  CONCLUSIONS
  Certain cytokines, such as IL-10 and TNF-alpha, might be expressed preferentially in EBV positive peripheral T cell lymphomas. It is likely that such a cytokine environment enhances EBV infection and contributes towards tumorigenesis.
authors.affiliation: Department of Pathology, University of Hong Kong, People's Republic of China.
authors.forename: J W
authors.initials: JW
authors.lastname: Ho
authors.forename: R H
authors.initials: RH
authors.lastname: Liang
authors.forename: G
authors.initials: G
authors.lastname: Srivastava
mesh_terms: D016207:Cytokines / Q000378:metabolism*; D020031:Epstein-Barr Virus Infections / Q000150:complications / Q000276:immunology*; D004854:Herpesvirus 4, Human / Q000302:isolation & purification*; D006801:Humans; D016753:Interleukin-10 / Q000378:metabolism; D007694:Killer Cells, Natural / Q000473:pathology; D016411:Lymphoma, T-Cell, Peripheral / Q000276:immunology* / Q000821:virology*; D012260:Ribonucleases; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D012260:Ribonucleases