Sonia Benhamida

Publications (2)16.55 Total impact

• Source

  Available from: ncbi.nlm.nih.gov

  Article: Human CD34+ cells differentiate into microglia and express recombinant therapeutic protein.

  Muriel Asheuer, Françoise Pflumio, Sonia Benhamida, Anne Dubart-Kupperschmitt, Françoise Fouquet, Yoshinori Imai, Patrick Aubourg, Nathalie Cartier
  [show abstract] [hide abstract]
  ABSTRACT: In rodents, bone marrow-derived cells enter the brain during adult life. Allogeneic bone marrow transplantation is used to treat genetic CNS diseases, but the fate of human bone marrow and CD34(+) cells within the brain remains to be elucidated. The present study demonstrates that cells derived from human CD34(+) cells, isolated from either cord blood or peripheral blood, migrate into the brain after infusion into nonobese diabetic/severe combined immunodeficient mice. Both types of CD34(+)-derived cells differentiate into perivascular and ramified microglia. The lentiviral transfer of genes into CD34(+) cells before infusion does not modify the differentiation of human CD34(+) cells into microglia, allowing new transgenic proteins to be expressed in these cells. The transplantation of CD34(+) cells could thus be used for the treatment of CNS diseases.
  Proceedings of the National Academy of Sciences 04/2004; 101(10):3557-62. · 9.68 Impact Factor
• Article: Transduced CD34+ cells from adrenoleukodystrophy patients with HIV-derived vector mediate long-term engraftment of NOD/SCID mice.

  Sonia Benhamida, Françoise Pflumio, Anne Dubart-Kupperschmitt, Jing Chao Zhao-Emonet, Marina Cavazzana-Calvo, Francis Rocchiccioli, Serge Fichelson, Patrick Aubourg, Pierre Charneau, Nathalie Cartier
  [show abstract] [hide abstract]
  ABSTRACT: X-linked adrenoleukodystrophy (ALD), an inherited demyelinating disorder of the central nervous system, can be corrected by allogeneic bone marrow transplantation, likely due to the turnover of brain macrophages that are bone marrow derived. ALD is characterized by an accumulation of very long chain fatty acids (VLCFA) due to the deficiency of an ATP binding cassette transporter that imports these fatty acids in peroxisomes. Murine retroviral transduction results in metabolic correction of ALD CD34(+) cells in vitro but reinfusion of these cells into ALD patients would not provide clinical benefit owing to the absence of selective advantage conferred by transgene expression. High-efficiency transduction of ALD CD34(+) peripheral blood mobilized cells was achieved using an HIV-based vector driving ALD gene expression under the elongation factor 1 alpha promoter and a protocol without prestimulation of CD34(+) cells with cytokines prior to transduction to preserve their stem cell properties. Efficient expression of the ALD gene was demonstrated in monocytes/macrophages derived from cultures of transduced ALD CD34(+) cells and in long-term culture initiating cells. VLCFA metabolism was corrected in transduced CD34(+), CFU-derived, and LTC-derived cells, indicating that the vector-encoded ALD protein was fully functional. Transplantation of transduced ALD CD34(+) cells into NOD/SCID mice resulted in long-term expression of ALD protein in monocytes/macrophages derived from engrafted stem cells.
  Molecular Therapy 04/2003; 7(3):317-24. · 6.87 Impact Factor