ArticleRheumatology (Oxford, England)2025
Impaired humoral and T helper cell responses to toxic shock syndrome toxin-1 (TSST-1) in granulomatosis with polyangiitis.
Article in Rheumatology (Oxford, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesNasal carriage of toxic shock syndrome toxin-1 (TSST-1)-positive Staphylococcus aureus (SA) is associated with a high relapse rate in granulomatosis with polyangiitis (GPA), suggesting TSST-1's role in disease progression. This study investigated the immune response to S. aureus-derived TSST-1 and characterized TSST-1-specific Th cells in GPA patients.
methodsPlasma anti-TSST-1 IgG levels were measured in 45 remission GPA patients and 25 healthy controls (HCs) using ELISA. Circulating TSST-1-reactive CD4+T helper (Vβ2+Th) cells were analysed and sub-classified in 62 remission GPA patients and 22 HCs by flow cytometry. Additionally, PBMCs were stimulated in vitro with TSST-1 for 14 days to evaluate its effect on PR3-ANCA production and CD4+Th cell cytokine production (IFNγ, IL-4, IL-17, IL-21) measured by Phadia ImmunoCAP®250 and flow cytometry, respectively.
resultsGPA patients with nasal SA carriage (SA+) had lower plasma anti-TSST-1 IgG levels and reduced numbers of circulating Vβ2+Th cells compared with HCs. An increased frequency of Vβ2+Th cells expressing the phenotype of peripheral helper T cells (TPh; PD-1HighCXCR5Neg) was observed in SA+ GPA patients compared with HCs. TSST-1 stimulation enhanced IL-21 production in Th cells from SA+ patients and induced PR3-ANCA production in vitro in a subset of GPA patients. Notably, numbers of circulating Vβ2+Th cells correlated positively with increased relapse-free survival in SA+ GPA patients.
conclusionImpaired humoral immunity against Vβ2-restricted superantigens in SA+ GPA patients may lead to insufficient clearance of TSST-1. TSST-1-driven IL-21 production could enhance ANCA production and promote disease progression. Reduced Vβ2+Th cells may increase relapse risk, emphasizing their potential value as a tool for monitoring disease progression.
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