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*
Department of Clinical Immunology, Royal Free and University College Medical School, London, United Kingdom;
Department of Immunology, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom;
Division of Immunity and Infection, Birmingham University Medical School, United Kingdom; and
§
Department of Immunopathology, Glaxo-Wellcome Medicines Research Centre, Stevenage, United Kingdom
Anergic T cells have immunoregulatory activity and can survive for
extended periods in vivo. It is unclear how anergic T cells escape from
deletion, because both anergy and apoptosis can occur after TCR
ligation. Stimulation of human CD4+ T cell clones reactive
to influenza hemagglutinin peptides can occur in the absence of APCs
when MHC class II-expressing, activated T cells present peptide to each
other. This T:T peptide presentation can induce CD95-mediated
apoptosis, while the cells that do not die are anergic. We found that
the death after peptide or anti-CD3 treatment of a panel of
CD4+ T cell clones is blocked by IFN-ß secreted by
fibroblasts and also by IFN-
. This increases cell recovery after
stimulation, which is not due to T cell proliferation. This mechanism
for apoptosis inhibition rapidly stops protein kinase C-
translocation from the cytoplasm to the nucleus, which is an early
event in the death process. A central observation was that
CD4+ T cells that are rescued from apoptosis after T:T
presentation of peptide by IFN-ß remain profoundly anergic to
rechallenge with Ag-pulsed APCs. However, anergized cells retain the
ability to respond to IL-2, showing that they are nonresponsive but
functional. The prevention of peptide-induced apoptosis in activated T
cells by IFN-ß is a novel mechanism that may enable the survival
and maintenance of anergic T cell populations after TCR engagement.
This has important implications for the persistence of anergic T cells
with the potential for immunoregulatory function in
vivo.
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