Sjögren's disease & overlap diseases
Novel clinical phenotype-based stratification identifies distinct immunopathological and ultrasonographic signatures in Sjögren’s disease
Authors' conclusion
SjD clinical phenotypes exhibit distinct immunopathological and structural features. BALS is characterized by greater B cell infiltration and more pronounced parotid involvement, whereas LSAHS shows a closer association between T cell infiltration and glandular stiffness.
Study context
- Population
- Patients with Sjögren's disease (SjD) classified into clinically defined subgroups
- Participants
- 120 patients
- Exposure
- BALS vs high systemic activity (HSA) vs LSAHS clinical phenotypes of SjD
- Outcome
- Glandular immune composition (IHC of labial salivary gland biopsies for CD3⁺ T cells, CD20⁺ B cells, CD45⁺ leucocytes) and structural involvement (SGUS score, SWE shear wave velocity in major salivary glands)
Methodological detailsquantitative immunohistochemistry (IHC), salivary gland ultrasonography (SGUS) (OMERACT scoring), shear wave elastography, Spearman correlation analyses
- Quantitative IHC
- SGUS (OMERACT scoring)
- Shear wave elastography
- Spearman correlation analyses
Main finding
As reported in the abstract
Glandular immunopathology and structural involvement by phenotype
- BALS showed more severe glandular involvement, with higher frequencies of focus score ≥3 and SGUS score ≥2
- Increased CD20⁺ B cell infiltration in BALS vs LSAHS
- Elevated parotid stiffness (shear wave elastography (SWE)) in BALS
- Overall cohort: parotid stiffness correlated positively with CD3⁺, CD20⁺ and CD45⁺ infiltration
Observational data: associations, not effects.
Further findings
Parotid stiffness correlations by subgroup
- Parotid stiffness associated with CD20⁺ B cells in BALS
- Correlations with CD3⁺ T cells and CD45⁺ leucocytes observed only in LSAHS
Original publication
Novel clinical phenotype-based stratification identifies distinct immunopathological and ultrasonographic signatures in Sjögren’s disease. Rheumatology (Oxford). Published 14 August 2026. doi:10. 1093/ rheumatology/ keag423
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