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Prepublished online as a Blood First Edition Paper on December 27, 2002; DOI 10.1182/blood-2002-08-2574.
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Blood, 1 May 2003, Vol. 101, No. 9, pp. 3543-3549
IMMUNOBIOLOGY
CD28 loss in senescent CD4+ T cells: reversal by
interleukin-12 stimulation
Kenneth J. Warrington,
Abbe
N. Vallejo,
Cornelia M. Weyand, and
Jörg J. Goronzy
From the Departments of Medicine and Immunology, Mayo
Clinic, Rochester, MN.
CD28 is the quintessential costimulatory molecule expressed on
CD4+ and CD8+ T cells. During chronic
infections and the normal aging process, CD28 expression is lost,
compromising the functional activity of T cells. CD28 loss is promoted
by replicative stress, particularly in the presence of tumor necrosis
factor- , owing to an inoperative CD28 initiator element. It is
currently unknown whether CD28 loss is irreversible. The present study
examined cytokines for their ability to reinduce CD28 expression.
CD4+CD28null T cells constitutively expressed
interleukin-12 (IL-12) and  receptors, which were functional and
allowed for the up-regulation of the signal transducer and activator of
transcription-4 (STAT-4)-dependent gene CD161. Costimulation
of the T-cell and IL-12 receptors induced the transcription of CD28 in
approximately 50% of CD4+CD28null T-cell
clones and lines. IL-12 by itself did not restore CD28 expression.
Up-regulation of CD28 after IL-12 exposure correlated with the
reassembly of the CD28-initiator protein complex. The re-expressed
CD28 was functional and restored the ability of
CD4+CD28null T cells to express CD25 and CD40
ligand. Our data suggest that IL-12 may, in part, functionally rescue
senescent CD4+ T cells.
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