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J Interferon Cytokine Res. 2006 Jun;26(6):421-9.

IFN-alpha sensitizes daudi B lymphoma cells to anti-IgM induced loss of mitochondrial membrane potential through activation of c-Jun NH(2)-terminal kinase.

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Department of Immunology and Intractable Immune System Disease Research Center, Tokyo Medical University, Tokyo 160-8402, Japan.


Interferon-alpha (IFN-alpha) regulates multiple biologic functions, including antiviral activity, immune regulation, cell differentiation, and cell survival or death, in a variety of cell types. We and others have recently demonstrated that IFN-alpha induces cell death through activation of c-Jun NH(2)-terminal kinase (JNK) in human Daudi B lymphoma and U266 myeloma cells. Moreover, the IFN-alpha-induced signaling pathway has been shown to cross talk with the antigen receptor-mediated signaling cascade. In the present study, we examined whether IFN-alpha affects cell death after engagement of membrane immunoglobulin (mIg) using anti-IgM. Daudi cells pretreated with low concentrations of IFN-alpha (25 or 250 U/mL) for 24 h were stimulated with anti-IgM (1-10 microg/mL) for 24 h. The cells were assayed for JNK activation, mitochondrial membrane potential (DeltaPsim) by Western blotting, and DiOC(6) staining, respectively. The IFN-alpha-primed Daudi cells showed an increased sensitivity to subsequent stimulation with anti-IgM, as assessed by JNK activation and DeltaPsim. Moreover, Daudi cells overexpressing the constitutively active or dominant-negative form of JNK were substantially susceptible or resistant to anti-IgM-induced DeltaPsim, respectively, compared with cells overexpressing the control vector alone. Taken together, these results indicate that IFN-alpha renders Daudi B lymphoma cells susceptible to anti-IgM-induced apoptosis, probably through upregulation of JNK activation.

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