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Modulation of hematopoiesis in mice with a truncated mutant of the
interleukin-2 receptor gamma chain
K Ohbo, T Suda, M Hashiyama, A Mantani, M Ikebe, K Miyakawa, M Moriyama, M Nakamura, M Katsuki, K Takahashi, K Yamamura and K Sugamura
Department of Microbiology, Tohoku University School of Medicine, Sendai,
Japan.
The interleukin-2 (IL-2) receptor gamma chain is indispensable for IL-2- ,
IL-4-, IL-7-, IL-9-, and IL-15-mediated signaling. Mutations of the human
gamma chain cause the X-linked severe combined immunodeficiency (XSCID),
showing that T and natural killer cells absolutely require the gamma chain
for their development in humans. To elucidate the roles of the gamma chain
in hematopoiesis, we have generated mice, by gene targeting, that express a
form of the gamma chain lacking the cytoplasmic region. Male mice carrying
the truncated gamma-chain mutant, which mimics mutations in patients with
XSCID, showed a decrease in the number of lymphocytes and an increase in
monocytes; the number of T cells was profoundly reduced and no natural
killer cells were detected, which is similar to the characteristic of human
XSCID. Unlike human XSCID, the levels of B cells were also reduced. In
spite of the severe decrease in CD45R+/sIgM+ B cells, the level of IgM in
serum of the 8-week-old mutant mice was higher than that of control
littermates. Interestingly, the stem cell population with surface
phenotypes of CD34, c-kit, and Sca-1 was significantly increased.
Furthermore, the colony-forming assay showed that the mutant mice had
15-fold higher numbers of hematopoietic progenitor cells in the spleen as
compared with that of controls. These results indicate that functional loss
of the gamma chain causes significant effects on the immunological system
in mice.
Volume 87,
Issue 3,
pp. 956-967,
02/01/1996
Copyright © 1996 by The American Society of Hematology
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