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Blood, 15 January 2002, Vol. 99, No. 2, pp. 513-519
HEMATOPOIESIS
Enforced expression of the Ikaros isoform IK5 decreases the
numbers of extrathymic intraepithelial lymphocytes and natural
killer 1.1+ T cells
Sean N. Tucker,
Heidi K. Jessup,
Hodaka Fujii, and
Christopher B. Wilson
From the Departments of Immunology and Pediatrics,
University of Washington, Seattle; and the Basel Institute for
Immunology, Switzerland.
The zinc-finger protein Ikaros plays an important role in lymphoid
homeostasis, and loss of Ikaros expression through germline disruption
impairs lymphoid development. However, the role played by Ikaros after
commitment to the T-cell lineage is unclear. To address this question,
this study used the lck proximal promoter to drive the expression in
T-cell progenitors of a naturally occurring short Ikaros isoform (IK5),
which lacks the DNA-binding domain, reasoning that IK5 will form
heterodimers with long isoforms and perturb their function. The IK5
transgene led to a selective and dramatic decrease in extrathymic
intestinal intraepithelial lymphocytes (IELs) and natural
killer 1.1+ T (NK T) cells with little effect on
conventional   T cells, which resembles the T-cell phenotype of
interleukin-15 receptor chain (IL-15R) and IL-2/IL-15 receptor
chain (IL-2R) knockout mice. The expression of IL-2R on
double-negative T-cell progenitors of bi-5 was reduced, but enforced
expression of IL-2R did not rescue IELs or NK T cells in bi-5
transgenic mice, suggesting that Ikaros or Ikaros family members
regulate the expression of additional genes that are essential for the
development of IELs and NK T cells. The study concludes that modest
changes in the ratio of short to long Ikaros isoforms can substantially
perturb T-cell development, and the development of IELs and NK T cells is particularly sensitive to such changes.
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