This article is part of the Research Topic PI3K signalling (Frontiers in B Cell Biology)

Review ARTICLE

Front. Immunol., 06 August 2012 | http://dx.doi.org/10.3389/fimmu.2012.00228

Akt and mTOR in B cell activation and differentiation

  • Department of Molecular Biology and Biochemistry, Institute for Immunology, University of California Irvine, Irvine, CA, USA

Activation of phosphoinositide 3-kinase (PI3K) is required for B cell proliferation and survival. PI3K signaling also controls key aspects of B cell differentiation. Upon engagement of the B cell receptor (BCR), PI3K activation promotes Ca2+ mobilization and activation of NFκB-dependent transcription, events which are essential for B cell proliferation. PI3K also initiates a distinct signaling pathway involving the Akt and mTOR serine/threonine kinases. It has been generally assumed that activation of Akt and mTOR downstream of PI3K is essential for B cell function. However, Akt and mTOR have complex roles in B cell fate decisions and suppression of this pathway can enhance certain B cell responses while repressing others. In this review we will discuss genetic and pharmacological studies of Akt and mTOR function in normal B cells, and in malignancies of B cell origin.

Keywords: B cells, proliferation, differentiation, antibody, PI3K, Akt, mTOR, kinase

Citation: Limon JJ and Fruman DA (2012) Akt and mTOR in B cell activation and differentiation. Front. Immun. 3:228. doi: 10.3389/fimmu.2012.00228

Received: 01 May 2012; Paper pending published: 25 May 2012;
Accepted: 14 July 2012; Published online: 06 August 2012.

Edited by:

Klaus Okkenhaug, Babraham Institute, UK

Reviewed by:

Michael R. Gold, The University of British Columbia, Canada
John D. Colgan, University of Iowa, USA
David Nemazee, The Scripps Research Institute, USA

Copyright: © 2012 Limon and Fruman. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.

*Correspondence: David A. Fruman, Department of Molecular Biology and Biochemistry, University of California Irvine, 3242 McGaugh Hall, Irvine, CA 92697-3900, USA. e-mail: dfruman@uci.edu