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Abnormal Myelocytic Cell Development in Interleukin-2
(IL-2)-Deficient Mice: Evidence for the Involvement of IL-2 in
Myelopoiesis
Tannishtha Reya,
Nikhat V. Contractor,
Matthew S. Couzens,
Mariusz
A. Wasik,
Stephen G. Emerson, and
Simon R. Carding
From the Departments of Microbiology, Medicine, Pathology and
Laboratory Medicine, Division of Hematology and Oncology, University of
Pennsylvania School of Medicine, Philadelphia, PA.
Mice lacking interleukin-2 (IL-2) developed a severe hematopoietic
disorder characterized by the abnormal development of myeloid cells and
neutropenia. Analysis of the bone marrow of IL-2-deficient (IL-2 /) mice showed that the number of mature
polymorphonuclear cells was decreased by 65% to 75%, and
granulocyte/macrophage precursor cells were reduced by 50%. Bone
marrow cells from IL-2/ mice were unable to sustain
myelopoiesis in lethally irradiated mice and in long-term bone marrow
cultures (LTBMC). The addition of exogenous IL-2 to LTBMC of
IL-2/ cells partially restored hematopoietic
progenitor activity. In the bone marrow of wild-type mice, immature
(Mac-1lo) myeloid cells, including myeloblasts and
promyelocytes, constitutively expressed the  -chain of the IL-2R, and
the number of Mac-1loIL-2R+ cells was
increased by twofold to threefold in IL-2/ mice.
During culture in the presence of IL-2 and the absence of stromal
cells, Mac-1loIL-2R+ immature myeloid
cells proliferated and gave rise to mature granulocytes and
macrophages. Collectively, these observations indicate that defective
myelopoiesis in IL-2/ mice is at least in part a
consequence of their direct dependency on IL-2, and by regulating the
growth of immature myeloid cells, IL-2 plays an important role in the
homeostatic regulation of myelocytic cell generation.
Blood, Vol. 91 No. 8 (April 15), 1998:
pp. 2935-2947
© 1998 by The American Society of Hematology.
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