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Activation of class I HLA expression by TNF‐alpha and gamma‐interferon is mediated through protein kinase C‐dependent pathway in CML cell lines
Author(s) -
Seong David,
Sims Simon,
Johnson Elizabeth,
Lyding Judith,
Lopez Alfredo,
Garovoy Marvin,
Talpaz Moshe,
Kantarjian Hagop,
LopezBerestein Gabriel,
Reading Christopher,
Deisseroth Albert
Publication year - 1991
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1991.tb04449.x
Subject(s) - interferon gamma , alpha interferon , interferon , human leukocyte antigen , microbiology and biotechnology , biology , protein kinase a , tumor necrosis factor alpha , cancer research , chronic myelogenous leukemia , immunology , kinase , antigen , cytokine , leukemia
Summary. The combination of tumour necrosis factor alpha (TNFα) and gamma‐interferon induced transcription of class I HLA genes in chronic myelogenous leukaemia (CML) cell lines through the formation of a complex between nuclear proteins and the transcriptional enhancers associated with these genes. Although gamma‐interferon or TNF‐alpha stimulated expression of class I HLA antigens in the EM2 and K562 CML cell lines when used alone, the effect of the combination of TNF‐alpha and gamma‐interferon was greater than that observed with either agent alone. The induction of class I HLA expression by gamma‐interferon and TNF‐alpha was inhibited completely by the isoquinoline sulfonamide H7, an inhibitor of protein kinase C. We conclude that the enhancement of the gamma‐interferon induced transcriptional activation of class I HLA gene expression by TNF‐alpha involves a protein kinase C‐dependent pathway.