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Blood, 15 February 2001, Vol. 97, No. 4, pp. 1027-1034
IMMUNOBIOLOGY
Cell-surface trafficking and release of flt3 ligand from T
lymphocytes is induced by common cytokine receptor  -chain signaling
and inhibited by cyclosporin A
Elena Chklovskaia,
Catherine Nissen,
Lukas Landmann,
Christoph Rahner,
Otmar Pfister, and
Aleksandra Wodnar-Filipowicz
From the Department of Research, University Hospital
Basel, and Institute of Anatomy, University of Basel, Basel,
Switzerland.
The flt3 ligand (FL) is a growth and differentiation factor for
primitive hematopoietic precursors, dendritic cells, and natural killer
cells. Human T lymphocytes express FL constitutively, but the cytokine
is retained intracellularly within the Golgi complex. FL is mobilized
from the cytoplasmic stores and its serum levels are massively
increased during the period of bone marrow aplasia after stem cell
transplantation (SCT). Signals that trigger the release of FL by T
cells remain unknown. This study shows that interleukin (IL)-2, IL-4,
IL-7, and IL-15, acting through a common receptor  chain (c), but
not cytokines interacting with other receptor families, are efficient
inducers of cell surface expression of membrane-bound FL (mFL) and
secretion of soluble FL (sFL) by human peripheral blood T lymphocytes.
The c-mediated signaling up-regulated FL in a T-cell
receptor-independent manner. IL-2 and IL-7 stimulated both FL messenger
RNA (mRNA) expression and translocation of FL protein to the cell
surface. Cyclosporin A (CsA) inhibited c-mediated trafficking of FL
at the level of transition from the Golgi to the trans-Golgi network.
Accordingly, serum levels of sFL and expression of mFL by T cells of
CsA-treated recipients of stem cell allografts were reduced
approximately 2-fold (P < .01) compared to patients
receiving autologous grafts. The conclusion is that FL expression is
controlled by c receptor signaling and that CsA interferes with FL
release by T cells. The link between c-dependent T-cell activation
and FL expression might be important for T-cell effector functions in
graft acceptance and antitumor immunity after SCT.
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