Suppressor aß T Lymphocytes Control Innate Resistance to Endotoxic Shock

A considerable amount of research has focused on elucidating the mechanisms by which cytokines synthesized by cells of the innate immune system participate in the life-threatening multiple-organ failure of endotoxic shock. We show here that αβ T cells, which are archetypes of the adaptive cellular i...

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Bibliographic Details
Published in:The Journal of infectious diseases 2005-09, Vol.192 (6), p.1039-1046
Main Authors: Jones-Carson, Jessica, Fantuzzi, Giamila, Siegmund, Britta, Dinarello, Charles, Tracey, Kevin J., Wang, Haichao, Fang, Ferric C., Vazquez-Torres, Andres
Format: Article
Language:English
Subjects:
Bacteria
Cytokines
Endotoxemia
Interferons
Lipopolysaccharides
Mice
Receptors
Septic shock
T lymphocytes
Toll like receptors
Tumor necrosis factors
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Summary:A considerable amount of research has focused on elucidating the mechanisms by which cytokines synthesized by cells of the innate immune system participate in the life-threatening multiple-organ failure of endotoxic shock. We show here that αβ T cells, which are archetypes of the adaptive cellular immune response, suppress the proinflammatory cascade triggered during the early stages of lipopolysaccharide (LPS)-induced endotoxemia. The absence of αβ T cells led to the fulminant death of LPS-challenged mice, coinciding with a massive release of the proinflammatory cytokines tumor necrosis factor (TNF)-α and interferon (IFN)-γ and a marked reduction in the synthesis of the immunosuppressive cytokine transforming growth factor (TGF)-β. Cytotoxic T lymphocyte antigen (CTLA)-positive αβ T cells emerging shortly after LPS challenge appear to control TGF-β synthesis. The neutralization of either TGF-β or CTLA4 resulted in similar increases in IFN-γ and TNF-α serum concentrations in LPS-challenged mice. These observations suggest that suppressor aαβ T lymphocytes protect against the proinflammatory cascade unleashed during the innate stages of endotoxemia.
ISSN:0022-1899