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The Journal of Immunology, 2001, 167: 6366-6373.
Copyright © 2001 by The American Association of Immunologists

The Association of Aiolos Transcription Factor and Bcl-xL Is Involved in the Control of Apoptosis

Angelita Rebollo1, Verónica Ayllón, Aarne Fleischer, Carlos Martínez-A. and Angel Zaballos

Centro Nacional de Biotecnología, Department of Immunology and Oncology, Campus de Cantoblanco, Universidad Autónoma de Madrid, Madrid, Spain

We have analyzed the mechanism implicated in the control of the anti-apoptotic role of Bcl-xL. We show that IL-4 deprivation induces apoptosis, but does not modulate Bcl-xL expression. Because Bcl-xL does not promote cell survival in the absence of IL-4, we investigate the mechanism by which Bcl-xL was unable to inhibit apoptosis. Using yeast two-hybrid system, coimmunoprecipitation, and indirect immunofluorescence techniques, we found that Bcl-xL interacts with the transcription factor Aiolos in IL-4-stimulated cells, increasing upon IL-4 deprivation. IL-4 does not promote translocation of Aiolos or Bcl-xL, but induces tyrosine phosphorylation of Aiolos, which is required for dissociation from Bcl-xL. Transfection experiments confirm that cells overexpressing Bcl-xL are able to prevent apoptosis in the absence of IL-4. On the contrary, cells that overexpress Bcl-xL and Aiolos are unable to block apoptosis in the absence of IL-4. We propose a model for the regulation of the Bcl-xL anti-apoptotic role via Aiolos.




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