• Media type: E-Article
  • Title: Reprogramming IgH isotype-switched B cells to functional-grade induced pluripotent stem cells
  • Contributor: Wesemann, Duane R.; Portuguese, Andrew J.; Magee, Jennifer M.; Gallagher, Michael P.; Zhou, Xiaolong; Panchakshari, Rohit A.; Alt, Frederick W.
  • Published: National Academy of Sciences, 2012
  • Published in: Proceedings of the National Academy of Sciences of the United States of America, 109 (2012) 34, Seite 13745-13750
  • Language: English
  • ISSN: 0027-8424
  • Origination:
  • Footnote:
  • Description: Induced pluripotent stem cells (iPSCs) can be formed from somatic cells by a defined set of genetic factors; however, aberrant epigenetic silencing of the imprinted Dlk1-Dio3 gene cluster often hinders their developmental potency and ability to contribute to high-grade chimerism in mice. Here, we describe an approach that allows splenic B cells activated to undergo Ig heavy-chain (IgH) class-switch recombination (CSR) to be reprogrammed into iPSCs that contribute to high-grade chimerism in mice. Treatment of naïve splenic B cells in culture with anti-CD40 plus IL-4 induces IgH CSR from IgM to IgG1 and IgE. CSR leads to irreversible IgH locus deletions wherein the IgM-producing Cµ exons are permanently excised from the B-cell genome. We find that anti-CD40 plus IL-4-activated cells produce iPSCs that are uniformly hypermethylated in the imprinted Dlk1-Dio3 gene cluster and fail to produce chimerism in mice. However, treatment of activated cells with the methyltransferase inhibitor 5-aza-2'-deoxycytidine before and at early stages of reprogramming attenuates hypermethylation of the Dlk1-Dio3 locus in resultant iPSCs and enables them to form high-grade chimerism in mice. These conditions allowed us to produce chimeric mice in which all mature cells were derived entirely from IgG1-expressing B-cell-derived iPSCs. We conclude that culture conditions of activated cells before and at early stages of reprogramming influence the developmental potency of resultant iPSCs.
  • Access State: Open Access