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Open Access Green as soon as Postprint is submitted to ZB.
Transcriptional basis of lymphocyte tolerance.
Immunol. Rev. 210, 105-119 (2006)
Signaling through lymphocyte antigen receptors has the potential to
initiate several distinct outcomes: proliferation, differentiation,
apoptosis, or functional unresponsiveness. Expansion and differentiation
of effector T cells is required for defense against foreign antigens,
whereas functional unresponsiveness, termed anergy, is a cell-intrinsic
mechanism that contributes to peripheral self-tolerance. Other
mechanisms of peripheral tolerance include the 'dominant' tolerance
imposed by regulatory T cells and immunosuppression mediated by
interleukin-10 and transforming growth factor-beta. T- and B-cell
antigen receptor ligation induces an increase in intracellular calcium
levels as well as activating additional signaling pathways that are
further potentiated by costimulatory receptors. In this review, we argue
that cell-intrinsic programs of peripheral anergy and tolerance are
imposed by sustained calcium signaling in lymphocytes. We address in
particular the role of the calcium-dependent transcription factor
nuclear factor for activation of T cells, which is activated by antigen
receptor stimulation and, depending on the presence or absence of input
from its transcriptional partner, activator protein-1, dictates two
distinct transcriptional programs: activation or tolerance.
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Publication type
Article: Journal article
Document type
Scientific Article
ISSN (print) / ISBN
0105-2896
e-ISSN
1600-065X
Journal
Immunological Reviews
Quellenangaben
Volume: 210,
Pages: 105-119
Publisher
Wiley
Non-patent literature
Publications
Reviewing status
Peer reviewed