-transparent.png){kind=logo}
Adenosine deaminase (ADA) deficiency has been reported in association with severe combined immunodeficiency disease (SCID). The mechanism by which ADA deficiency causes immune dysfunction has been investigated in model systems to which the ADA inhibitor deoxycoformycin (dCf) had been added. Previously, we demonstrated that dCF did not prevent proliferation and differentiation of myeloid and lymphoid stem cells. We have now shown that addition of deoxyadenosine to dCf-containing cultures inhibited proliferation of hemopoietic stem cells. This inhibition was, however, equally effective for both normal myeloid and lymphoid stem cells. These findings suggest that other differences may exist between SCID myeloid and lymphoid stem cells to account for the relative sparing of myelopoiesis in SCID patients.
M T Aye, and
J V Dunne, and
W C Yang
February 1988,
Human immunology,
M T Aye, and
J V Dunne, and
W C Yang
August 1982,
British journal of haematology,
M T Aye, and
J V Dunne, and
W C Yang
April 1982,
Biochemical pharmacology,
M T Aye, and
J V Dunne, and
W C Yang
June 1990,
Journal of cellular biochemistry,
M T Aye, and
J V Dunne, and
W C Yang
September 1989,
Bone marrow transplantation,
M T Aye, and
J V Dunne, and
W C Yang
September 1997,
Biochemical and biophysical research communications,
M T Aye, and
J V Dunne, and
W C Yang
July 1979,
Journal of immunology (Baltimore, Md. : 1950),
M T Aye, and
J V Dunne, and
W C Yang
February 1992,
Thymus,
M T Aye, and
J V Dunne, and
W C Yang
July 1985,
Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society,
M T Aye, and
J V Dunne, and
W C Yang
January 1985,
Cancer investigation,
