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Hematopoiesis in mice lacking the entire granulocyte-macrophage colony-
stimulating factor/interleukin-3/interleukin-5 functions
R Nishinakamura, A Miyajima, PJ Mee, VL Tybulewicz and R Murray
DNAX Research Institute, Palo Alto, CA 94304-1104, USA.
Interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor
(GM-CSF), and IL-5 are major hematopoietic cytokines produced by activated
T cells and exhibit similar biologic activities by signaling through a
common receptor subunit (beta c). Mice lacking beta c show a pulmonary
alveolar proteinosis-like disease and reduced numbers of peripheral
eosinophils, which are explained by the lack of GM-CSF and IL-5 function,
respectively. However, beta c-deficient hematopoietic cells do respond to
IL-3 normally, probably through an additional beta subunit of the IL-3
receptor (beta IL3) that is present in the mouse. Thus, almost normal
hematopoiesis in beta c-deficient mice may be caused by functional
redundancy between IL-3 and GM-CSF. To clarify the role of the entire
IL-3/GM-CSF/IL-5 system in hematopoiesis in vivo, we crossed the beta c
mutant mice with mice deficient for IL-3 ligand to generate mice lacking
the entire IL-3/GM-CSF/IL-5 functions. The double- mutant mice were
apparently normal and fertile. The severity of the lung pathology in the
beta c/IL-3 double-mutant mice showed normal hemodynamic parameters except
for reduced numbers of eosinophils and the lack of eosinophilic response to
parasites, which were also found in beta c mutant mice. The immune response
of the beta c/IL-3 double- mutant mice to Listeria mono-cytogenes was
normal, as was hematopoietic recovery after administration of the cytotoxic
drug, 5-fluorouracil. Although it has been believed that IL-3/GM-CSF/IL-5
produced by activated T cells play a major role in expansion of
hematopoietic cells in emergency, our results indicate that the entire
function of IL-3/GM- CSF/IL-5 is dispensable for hematopoiesis in emergency
as well as in the steady state. Thus, there must be an alternative
mechanism to produce blood cells in both situations.
Volume 88,
Issue 7,
pp. 2458-2464,
10/01/1996
Copyright © 1996 by The American Society of Hematology
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