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Preferential type 1–1 cytokine gene expressions in peripheral T‐cell lymphomas
Author(s) -
Ho Joanna W. Y.,
Liang Raymond H. S.,
Srivastava Gopesh
Publication year - 1999
Publication title -
hematological oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 44
eISSN - 1099-1069
pISSN - 0278-0232
DOI - 10.1002/(sici)1099-1069(199909)17:3<117::aid-hon640>3.0.co;2-1
Subject(s) - cytokine , interleukin 4 , immunology , tumor necrosis factor alpha , interleukin 10 , lymphoma , medicine , biology
In this study, we have investigated whether a pattern of cytokine gene expression can be found in non‐Hodgkin's peripheral T‐cell lymphoma (PTCL). By using RNase protection assays and RT‐PCR, we have systematically studied IL1α, IL1β, IL1‐Ra, IL2, IL4, IL5, IL6, IL9, IL10, IL12p35, IL12p40, IL13, IL14, IL15, IFNγ, IFNβ, TNFα, TNFβ, LTβ, and TGFβ1, TGFβ2 and TGFβ3. Twenty‐two cases of PTCL inclusive of three nasal NK‐cell lymphomas were selected for the study; three cases of reactive lymphoproliferation were included for comparison. Results show that IFNγ gene expression (key Type 1 cytokine) was frequently detected [18/22 (82 per cent)]. In contrast, IL4 (key Type 2 cytokine) was only detected in 4/22 (18 per cent) of cases (weaker than IFNγ in three cases). This distinction was also found at the protein level by immunohistochemistry. In addition, TNFβ and TNFα (strongly expressed by Type 1 cells) were almost complimentarily detected [4/19 (21 per cent)] and 12/19 (63 per cent), respectively). In contrast, neither IL5 nor IL13 (strongly expressed by Type 2 cells) were detected at all. However, 14/22 cases expressed IL10, another Type 2 cytokine, which suggests that the autoregulatory feedback loop is stimulated. Compared to the tumour types, the cytokine profiles in the reactive lymphoproliferative types also resembled a Type 1‒like pattern but was less striking. The overall result suggested a preferential expression of certain cytokines, and these cytokines may play an important role in pathophysiologic progression in these T‐cell disorders. Copyright © 1999 John Wiley & Sons, Ltd.