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      Superantigens associated with staphylococcal and streptococcal toxic shock syndrome are potent inducers of tumor necrosis factor-beta synthesis.

      The Journal of Infectious Diseases
      Antigens, Bacterial, immunology, Bacterial Proteins, Bacterial Toxins, Cells, Cultured, Enterotoxins, Exotoxins, Humans, Leukocytes, Mononuclear, metabolism, Lymphotoxin-alpha, biosynthesis, Membrane Proteins, Shock, Septic, etiology, Staphylococcal Infections, Streptococcal Infections, Superantigens, Tumor Necrosis Factor-alpha

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          Abstract

          The role of tumor necrosis factor-alpha (TNF alpha) in the pathogenesis of severe bacterial infections has been studied extensively. However, the role of TNF beta, a lymphokine with biologic activities similar to those of TNF alpha, has received little attention. Therefore, the purpose of this study was to examine the production of TNF beta by peripheral blood mononuclear cells in response to lipopolysaccharide (LPS) and the superantigens staphylococcal toxic shock syndrome toxin 1 (TSST-1) and streptococcal pyrogenic exotoxin A (SPEA). Though LPS was a more potent inducer of TNF alpha than was TSST-1 or SPEA, TSST-1 and SPEA were both more potent inducers of TNF beta. The superantigens TSST-1 and SPEA were more potent inducers of total TNF (TNF alpha and TNF beta) than was LPS. These data suggest that the induction of TNF beta synthesis may be a unique pathway by which superantigens associated with severe streptococcal and staphylococcal infections mediate shock and multiorgan failure characteristic of toxic shock syndrome.

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