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Blood, 1 April 2002, Vol. 99, No. 7, pp. 2518-2525
IMMUNOBIOLOGY
CD43 polarization in unprimed T cells can be dissociated from
raft coalescence by inhibition of HMG CoA reductase
Elena Gubina,
Trina Chen,
Lei Zhang,
Elaine F. Lizzio, and
Steven Kozlowski
From the Division of Monoclonal Antibodies, Center for
Biologics Evaluation and Research, Food and Drug Administration,
Bethesda, MD.
Movement of T-lymphocyte cell surface CD43 is associated with both
antigen activation of T-cell clones and chemokine induction of
T-lymphocyte motility. Here, we demonstrate that CD43 movement away
from the site of T-cell receptor ligation occurs in unprimed CD4+ T cells as well as T-cell clones. The T-cell receptor
(TCR)-dependent movement of CD43 in unprimed T cells is associated with
a polarized morphology and CD43 accumulation at the uropods of the
cells, unlike that reported for primed T cells. The polarization of
CD43 has a requirement for Src kinases and occurs in conjunction with lipid raft coalescence. Thymocytes and T-cell hybridomas, cells that
have altered responses to TCR activation and lack lipid raft coalescence, do not polarize CD43 as readily as unprimed T cells. The
movement of CD43 depends on the cholesterol biosynthetic pathway enzyme
3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase. Blockade of
this enzyme can specifically prevent CD43 redistribution without
affecting cell shape polarization. The likely mechanism of this
alteration in CD43 redistribution is through decreased protein
prenylation because the cholesterol-dependent lipid rafts still
coalesce on activation. These findings suggest that the polarization of
cell shape, lipid raft coalescence, and CD43 redistribution on T-cell
activation have signaling pathway distinctions. Dissecting out the
relationships between various stages of molecular redistribution and
lymphocyte activation may facilitate fine-tuning of immunologic responses.
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