Staphylococcal superantigens evoke temporary and reversible T cell anergy, but fail to block the development of a bacterium specific cellular immune response

Heran Zhang, Ian R. Monk, Jessica Braverman, Claerwen M. Jones, Andrew G. Brooks, Timothy P. Stinear and Linda M. Wakim ()
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Heran Zhang: at the Peter Doherty Institute for Infection and Immunity
Ian R. Monk: at the Peter Doherty Institute for Infection and Immunity
Jessica Braverman: at the Peter Doherty Institute for Infection and Immunity
Claerwen M. Jones: Monash University
Andrew G. Brooks: at the Peter Doherty Institute for Infection and Immunity
Timothy P. Stinear: at the Peter Doherty Institute for Infection and Immunity
Linda M. Wakim: at the Peter Doherty Institute for Infection and Immunity

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Superantigens (sAgs) are bacterial virulence factors that induce a state of immune hyperactivation by forming a bridge between certain subsets of T cell receptor (TCR) β chains on T lymphocytes, and class II major histocompatibility complex (MHC-II) molecules; this cross-linking leads to indiscriminate T cell activation, cytokine storm and toxic shock. Here we show that sAg exposure drives the preferential expansion of naive and central memory T cell subsets, but not effector or resident memory T cells, which instead, hyper release pro-inflammatory cytokines. A targeted therapeutic approach to minimise cytokine release by effector memory T cells attenuated sAg-induced cytokine release. Irrespective of antigen experience, sAg activation does not render mature T cells permanently dysfunctional, and full restoration of effector function is observed following a transient and reversible anergy. Moreover, we show that in the face of sAg induced immune hyperactivation, an intact bacterium-specific CD4+ T cell response can be mounted.

Date: 2024
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DOI: 10.1038/s41467-024-54074-8

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