Aetiopathogenesis
Differential Th follicular cell subsets in minor salivary glands of patients with primary Sjögren's syndrome and systemic lupus erythematosus associated with Sjögren’s syndrome
G. Hernandez-Molina1, V. Soto-Abraham2, V. Zamora-Legoff3, J. Furuzawa-Carballeda4
- Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
- Department of Pathology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
- Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
- Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico. jfuruzawa@gmail.com
CER14962
2021 Vol.39, N°6 ,Suppl.133
PI 0049, PF 0056
Aetiopathogenesis
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PMID: 34596020 [PubMed]
Received: 03/07/2021
Accepted : 15/09/2021
In Press: 29/09/2021
Published: 15/12/2021
Abstract
OBJECTIVES:
T follicular helper cells (Tfh) have been recognised in minor salivary glands (MSG) of patients with primary Sjögren’s syndrome (pSS). Nevertheless, if the Tfh1, Tfh2, Tfh17, Tfr phenotype is different when comparing pSS and associated SS in systemic lupus erythematosus (SLE) is unknown.
METHODS:
We included MSG biopsies from 8 pSS, 8 SLE/SS patients, 7 SLE patients, and 2 non-SS sicca patients. To determine the subpopulation of Tfh, a double-staining procedure for transcription factor B cell lymphoma 6 (Bcl-6)+/IL-17A+, Bcl6+/IL-4+, Bcl6+/IFN-γ+, and Bcl6+/Foxp3+ cells was performed. We estimated the mean percentage of positively staining cells in four fields per sample.
RESULTS:
Tfh1, Tfh2, and Tfh17 cells were highly expressed in pSS compared with the rest of the groups; conversely, in patients with SLE/SS predominated, the Tfh17 and in SLE patients the Tfh1 cells. Regulatory Tfh cells (Tfr) were similar in pSS and the rest of the patients. However, the lowest frequency was found in the SLE group. A positive correlation was observed between anti-Ro/SSA autoantibody and Tfh17 subset (r=0.726, p=0.0001); and with the (Tfh2+Tfh17)/Tfh1 ratio (r=0.844, p<0.0001) in the MSG of patients with pSS.
CONCLUSIONS:
We showed a differential Tfh profile in primary SS and SLE with associated SS. Whether this Tfh differential profile participates in the increased risk of lymphoproliferative disease in pSS compared with associated SS, or other outcomes, is yet to be determined in future studies.