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Suppressor alphabeta T lymphocytes control innate resistance to endotoxic shock.
Title | Suppressor alphabeta T lymphocytes control innate resistance to endotoxic shock. |
Publication Type | Journal Article |
Year of Publication | 2005 |
Authors | Jones-Carson, J, Fantuzzi, G, Siegmund, B, Dinarello, C, Tracey, KJ, Wang, H, Fang, FC, Vazquez-Torres, A |
Journal | J Infect Dis |
Volume | 192 |
Issue | 6 |
Pagination | 1039-46 |
Date Published | 2005 Sep 15 |
ISSN | 0022-1899 |
Keywords | Animals, Disease Models, Animal, Endotoxemia, Immunity, Innate, Lipopolysaccharides, Mice, Mice, Inbred C57BL, Receptors, Antigen, T-Cell, alpha-beta, Shock, Septic, Survival Analysis, T-Lymphocytes, Regulatory, Transforming Growth Factor beta, Tumor Necrosis Factor-alpha |
Abstract | 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 alphabeta 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 alphabeta T cells led to the fulminant death of LPS-challenged mice, coinciding with a massive release of the proinflammatory cytokines tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma and a marked reduction in the synthesis of the immunosuppressive cytokine transforming growth factor (TGF)-beta. Cytotoxic T lymphocyte antigen (CTLA)-positive alphabeta T cells emerging shortly after LPS challenge appear to control TGF-beta synthesis. The neutralization of either TGF-beta or CTLA4 resulted in similar increases in IFN-gamma and TNF-alpha serum concentrations in LPS-challenged mice. These observations suggest that suppressor alphabeta T lymphocytes protect against the proinflammatory cascade unleashed during the innate stages of endotoxemia. |
DOI | 10.1086/432727 |
Alternate Journal | J. Infect. Dis. |
PubMed ID | 16107957 |
Grant List | AI10181 / AI / NIAID NIH HHS / United States AI15614 / AI / NIAID NIH HHS / United States AI39557 / AI / NIAID NIH HHS / United States AI54959 / AI / NIAID NIH HHS / United States DK061483 / DK / NIDDK NIH HHS / United States HL68743 / HL / NHLBI NIH HHS / United States R01 GM057226 / GM / NIGMS NIH HHS / United States |