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Blood, 15 May 2001, Vol. 97, No. 10, pp. 3152-3160
IMMUNOBIOLOGY
Red blood cells inhibit activation-induced cell death and
oxidative stress in human peripheral blood T lymphocytes
Ana Mafalda Fonseca,
Graça Porto,
Koji Uchida, and
Fernando A. Arosa
From the Laboratory of Molecular Immunology, Institute
for Molecular and Cell Biology, University of Porto; the Department of
Hematology, Santo António General Hospital, Porto, Portugal; and
the Laboratory of Food and Biodynamics, Nagoya University Graduate
School of BioAgricultural Sciences, Japan.
Red blood cells (RBCs) are known to perform one prominent function:
to carry and deliver oxygen to the tissues. Earlier studies, however,
suggested a role for RBCs in potentiating T-cell proliferation in
vitro. Here it is shown that the presence of RBCs in cultures of
stimulated human peripheral blood lymphocytes strengthens T-cell proliferation and survival. Analysis of phosphatidylserine
externalization and DNA fragmentation showed that RBCs inhibit T-cell
apoptosis. This inhibition correlated with a reduction in CD71 but not
CD95 expression. RBCs enhanced T-cell proliferation and survival upon activation with phytohemagglutinin and with OKT3 antibodies. Studies aimed at characterizing the cellular and molecular basis of the protection afforded to T cells by RBCs showed that (1) optimal protection required intact RBCs and red cell/T-cell contact but not
monocytes; (2) RBCs markedly reduced the level of intracellular reactive oxygen species; and (3) RBCs inhibited the formation of protein-bound acrolein, a peroxidation adduct in biologic systems. Overall, these data indicate that human RBCs protect T cells from activation-induced cell death, at least in part by reducing the pro-oxidant state, and suggest a role for RBCs as conceivable modulators of T-cell homeostasis.
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