Studies on the effect of deoxyadenosine on deoxycoformycin-treated myeloid and lymphoid stem cells.
نویسندگان
چکیده
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.
منابع مشابه
Conversion of a stem cell leukemia from a T-lymphoid to a myeloid phenotype induced by the adenosine deaminase inhibitor 2'-deoxycoformycin.
Selective failure of lymphoid development occurs in genetic deficiency of adenosine deaminase (ADA). We examined the in vivo effects of a potent inhibitor of ADA, 2'-deoxycoformycin, which was used to treat a patient with refractory acute leukemia. Unexpectedly, within 7 days of starting treatment, the leukemic phenotype underwent complete conversion from T lymphoblastic to promyelocytic, with ...
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ورودعنوان ژورنال:
- Blood
دوره 60 4 شماره
صفحات -
تاریخ انتشار 1982