Open AccessA tumour necrosis factor alpha autocrine loop contributes to proliferation and nuclear factor‐κB activation of Theileria parva ‐transformed B cells
Author(s) -
Guerg Julien,
Chaussepied Marie,
Sopp Paul,
Lizundia Regina,
Moreau MarieFrançoise,
Blumen Brigitte,
Werling Dirk,
Howard Christopher J.,
Langsley Gordon
Publication year - 2003
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1046/j.1462-5822.2003.00314.x
Subject(s) - autocrine signalling , biology , tumor necrosis factor alpha , microbiology and biotechnology , growth factor , cytokine , cell growth , cancer research , cell culture , immunology , receptor , biochemistry , genetics
Summary Theileria infection of bovine leucocytes induces uncontrolled proliferation and a transformed phenotype comparable to tumour cells. Infected cells have many characteristics of activated leucocytes and use autocrine loops to augment proliferation. We have shown previously that, in infected B cells, PI3‐K controls a granulocyte–macrophage colony‐stimulating factor (GM‐CSF) autocrine loop to increase both proliferation and activation of the activator protein 1 (AP‐1) transcription factor. We show here that the same infected B cells also use a tumour necrosis factor (TNF) alpha autocrine loop that again contributes to proliferation and augments nuclear factor (NF)‐κB activation. Interestingly, both pharmacological inhibition of TNF synthesis and neutralizing anti‐TNF antibodies lead to a reduction in proliferation and a 50% drop in NF‐κB activation, without inducing apoptosis.