Rapid and Rigorous IL-17A Production by a Distinct Subpopulation of Effector Memory T Lymphocytes Constitutes a Novel Mechanism of Toxic Shock Syndrome Immunopathology.

ABSTRACT: Toxic shock syndrome (TSS) is caused by staphylococcal and streptococcal superantigens (SAgs) that provoke a swift hyperinflammatory response typified by a cytokine storm. The precipitous decline in the host's clinical status and the lack of targeted therapies for TSS emphasize the need to identify key players of the storm's initial wave. Using a humanized mouse model of TSS and human cells, we herein demonstrate that SAgs elicit in vitro and in vivo IL-17A responses within hours. SAg-triggered human IL-17A production was characterized by remarkably high mRNA stability for this cytokine. A distinct subpopulation of CD4⁺ effector memory T (T_EM) cells that secrete IL-17A, but not IFN-γ, was responsible for early IL-17A production. We found mouse "T_EM-17" cell

SUBMITTER: Szabo PA 

PROVIDER: S-EPMC6635948 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature