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Apoptosis as a mechanism of T‐regulatory cell homeostasis and suppression
Author(s) -
Yolcu Esma S,
Ash Shifra,
Kaminitz Ayelet,
Sagiv Yuval,
Askenasy Nadir,
Yarkoni Shai
Publication year - 2008
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2008.62
Subject(s) - mechanism (biology) , homeostasis , microbiology and biotechnology , apoptosis , biology , genetics , physics , quantum mechanics
Activation‐induced cell death is a general mechanism of immune homeostasis through negative regulation of clonal expansion of activated immune cells. This mechanism is involved in the maintenance of self‐ and transplant tolerance through polarization of the immune responses. The Fas/Fas‐ligand interaction is a major common executioner of apoptosis in lymphocytes, with a dual role in regulatory T cell (Treg) function: Treg cell homeostasis and Treg cell‐mediated suppression. Sensitivity to apoptosis and the patterns of Treg‐cell death are of outmost importance in immune homeostasis that affects the equilibrium between cytolytic and suppressor forces in activation and termination of immune activity. Naive innate (naturally occurring) Treg cells present variable sensitivities to apoptosis, related to their turnover rates in tissue under steady state conditions. Following activation, Treg cells are less sensitive to apoptosis than cytotoxic effector subsets. Their susceptibility to apoptosis is influenced by cytokines within the inflammatory environment (primarily interleukin‐2), the mode of antigenic stimulation and the proliferation rates. Here, we attempt to resolve some controversies surrounding the sensitivity of Treg cells to apoptosis under various experimental conditions, to delineate the function of cell death in regulation of immunity.