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2V
2 T Cells Produce IFN- and TNF-
with an On/Off/On Cycling Pattern in Response to Live Bacterial Products1
Lymphocyte Biology Section, Division of Rheumatology, Immunology, and Allergy, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115
Whereas cytokine production in 
T cells is rapidly regulated
by exposure to peptide Ag, the mechanisms regulating cytokine
production by 
T cells are unknown. In this study, we demonstrate
that human V2V2 T cells produce IFN- and TNF- as early as
2 h after Ag exposure, and that they produce these cytokines in a
dose- and time- dependent manner in response to stimulation with a live
bacterial product, iso-butylamine (IBA), but not to dead
bacteria or LPS. T cells began, ceased, and then resumed IFN-
and TNF- generation in an on/off/on cycling pattern, both in vitro
and in vivo, depending on the presence or absence of IBA. IFN- and
TNF-, whose optimum production was dependent on IBA-stimulated
T cells, were critical for monocyte-mediated killing of
Escherichia coli. By limiting cytokine production to
periods of direct contact with live bacteria, T cells focus
their resources at the site of infection, while limiting systemic
immunopathology. Thus, human T cells may mediate innate
resistance to extracellular bacteria via tightly regulated cytokine
production without necessarily expanding in
number.
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