International Immunology, Vol 9, 945-953, Copyright © 1997 by Oxford University Press
N Van Houten, SF Blake, EJ Li, TA Hallam, DG Chilton, WK Gourley, LH Boise, CB Thompson and EB Thompson
Administration of glucocorticoids or exposure to ionizing radiation in vivo
results in a rapid cell death of thymocytes. We report that murine small
intestinal intraepithelial lymphocytes (IEL) are resistant to both steroid-
and radiation-induced deletion. This is due to resistance to apoptosis, as
evidenced by the absence of detectable apoptotic IEL nuclei in situ after
in vivo glucocorticoid treatment. IEL express normal levels of
glucocorticoid receptors and these receptors bind [3H]dexamethasone to
equivalent levels as other lymphocyte populations. Thus, their survival is
due to post-receptor signaling mechanisms. Many IEL express high levels of
Bcl-2 and that of these Bcl-2high IEL are largely TCR gamma delta +. Those
IEL that do express high levels of Bcl- 2 are CD8 alpha + beta - CD4-. In
addition, IEL express Bcl-x, another protein shown to be involved in the
protection of cells from apoptotic signals. IEL represent the first
lymphocyte population in vivo shown to have high levels of expression of
both molecules, that otherwise occur only in activated lymphocytes in
vitro. These data suggest that the Bcl- 2+Bcl-x+ IEL are activated cells
and not an effete population of cells necessarily destined to die. Also,
the high levels of Bcl-2 and Bcl-x in this in vivo activated population
supports the in vitro correlate of protection from activation-induced cell
death.
ARTICLES
Elevated expression of Bcl-2 and Bcl-x by intestinal intraepithelial lymphocytes: resistance to apoptosis by glucocorticoids and irradiation
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77555, USA.
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