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Blood, 15 December 2001, Vol. 98, No. 13, pp. 3562-3568
CHEMOKINES
Transgenic overexpression of the CC chemokine CCL21 disrupts
T-cell migration
Kent W. Christopherson II,
James J. Campbell, and
Robert
A. Hromas
From the Departments of Biochemistry/Molecular Biology
and Hematology/ Oncology, Indiana University Cancer Center, Indiana
University School of Medicine, Indianapolis; and Joint Program in
Transfusion Medicine, Children's Hospital, and Department of
Pathology, Harvard Medical School, Boston, MA.
Chemokines are a large family of cytokines that direct normal
leukocyte migration. They also have been implicated in leukocyte development and in the pathogenesis of many diseases. The CC chemokine CCL21, also known as Exodus-2, SLC, 6Ckine, and TCA4 induces both the
adhesion and migration of human T cells. CCL21 is hypothesized to
regulate the trafficking of T cells through secondary lymphoid tissues.
To test this hypothesis, a transgenic mouse model was generated that
placed the expression of mouse CCL21 (mCCL21) under the control of the
T cell-specific lck promoter to abrogate the concentration gradient to
which T cells normally respond. Overexpression of mCCL21 in T cells
resulted in defects in CCL21- and CCL19-induced T-cell chemotaxis, node
T-cell subpopulations, and lymph node architecture. The regulation of
T-cell trafficking in secondary lymphoid tissues by CCL21 is therefore
a tightly regulated system that can be altered by changes in the level
of environmental CCL21 protein.
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