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Abstract Number: 0889

Unraveling the Progression of Sjögren’s Disease at the Cellular and Histological Level Using Single-cell and Spatial Transcriptomics

Tomás Gomes1, Matilde Bandeira2, Rui do Amaral Vieira1, Bianca Correia1, Sofia Barreira3, Pedro Gaspar4, Rita Cruz-Machado5, Beatriz Filipe1, Pedro Ávila-Ribeiro1, Filipa Ribeiro1, Bruno Vidal1, Beatriz Val1, Filipa Costa6, Ana Teodósio Chícharo7, Augusto Silva1, Manuel Silvério-Antonio1, João Forjaz Lacerda1, João Eurico Fonseca1, Dolores López Presa8, Nikita Khmelinskii1, Saumya Kumar9, Luis Graca1 and Vasco C. Romão10, 1Instituto de Medicina Molecular (iMM Lisboa), Lisboa, Portugal, 2Centro Hospitalar Universitario Lisboa Norte, Lisboa, Portugal, 3Unidade Local de Saúde Santa Maria, Serviço de Reumatologia e Doenças Ósseas Metabólicas, Lisboa, Portugal, Lisbon, Portugal, 4Internal Medicine Department, Hospital Santa Maria, Unidade Local de Saúde Santa Maria, Lisbon, Portugal, Povoa de Santa Iria, Portugal, 5Unidade Local de Saúde Santa Maria, Serviço de Reumatologia e Doenças Ósseas Metabólicas, Lisboa, Portugal, Lisboa, Portugal, 6Rheumatology Department, Unidade Local de Saúde de Santa Maria. Rheumatology Research Unit, Instituto de Medicina Molecular João Lobo Antunes, Lisbon, Portugal, 7Unidade Local de Saúde do Algarve, Hospital de Faro, Faro, Portugal, Faro, Portugal, 8Pathology Department, Unidade Local de Saúde de Santa Maria, Lisbon Academic Medical Centre, Lisboa, Portugal, 9TWINCORE, a joint venture between the Helmholtz-Centre for Infection Research (HZI) and the Hannover Medical School (MHH), Hannover, Germany, Hannover, Germany, 10Rheumatology Department, ULS Santa Maria & Rheumatology Research Unit, Instituto Medicina Molecular, Faculty of Medicine, University of Lisbon, Lisbon, Portugal

Meeting: ACR Convergence 2024

Keywords: autoimmune diseases, Bioinformatics, genomics, Sjögren's syndrome

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Session Information

Date: Sunday, November 17, 2024

Title: Genetics, Genomics & Proteomics Poster

Session Type: Poster Session B

Session Time: 10:30AM-12:30PM

Background/Purpose: Sjögren’s Disease (SjD) is a systemic autoimmune disease that primarily targets salivary and lacrimal glands, causing tissue deterioration and loss of function. Disease progression depends on a plethora of scarcely explored cellular interactions. Over time, infiltrating immune cells organize into tertiary lymphoid structures (TLS) bearing self-reactive B cells. In some patients, this immune dysregulation ultimately leads to B cell lymphoma. However, the gene expression changes correlating with disease progression remain largely unknown. We aimed to elucidate the alterations in gene expression pathways and cellular heterogeneity in salivary glands of patients with SjD over the course of the disease, uncovering their association with disease phenotypes.

Methods: We recruited SjD patients at early (< 2 years since diagnosis) and late ( >10 years) disease stages. Minor salivary gland biopsies were collected from these patients. From those biopsies, we performed single-cell transcriptomics (scRNA-seq) and spatial transcriptomics (ST) (Fig. 1). Following quantification, scRNA-seq and ST data were analyzed using the Seurat R package.

Results: Analysis of scRNA-seq data from non-hematopoietic cells (sorted as CD45-) showed the cell types characteristic of normal human salivary glands (Fig.2 A and B). The hematopoietic cells sorted (as CD45+) from the same biopsies also showed a wide variety of cell types, with an abundance of plasma cells and various T cell populations (Fig.2 C and D).

Salivary gland cell types were mostly consistent between early and late donors. Fibroblast-like secretory pericytes were among those enriched in a late disease stage (Fig. 3A), and involved in more predicted cell-cell interactions compared to early donors (Fig. 3B). Salivary gland ST data from a late donor, showed that CCL19 (a chemoattractant ligand for CCR7, present in naïve T cells), was specifically expressed by fibroblast-like secretory pericytes (Fig. 2B), and present in and around areas of immune cell infiltration (Fig.3 C and D).

Conclusion: We generated a cell and tissue transcriptomic atlas of salivary glands from SjD patients at different disease stages. Our analyses revealed a wide range of cell types, including a fibroblast-like secretory pericyte population, and suggest that alterations to its abundance may have a pathogenical role in disease progression. The increased number of predicted cell-cell interactions and association with immune cell infiltrates further suggest a role for these cells in immune cell recruitment and TLS organization.

Supporting image 1

Fig. 1: Study design and data collection.

Supporting image 2

Fig. 2: Immune and stromal cell populations in salivary gland biopsied of Sjögren’s Disease (SjD) patients. (A) UMAP plot of scRNA-seq data from sorted non-hematopoietic cells (CD45-), highlighting the epithelial and stromal cell populations identified in 3 independent donors. (B) Selected genes for the main cell populations identified in A. (C) UMAP plot of scRNA-seq data from sorted hematopoietic cells (CD45+), highlighting the immune cell populations identified in 3 independent donors. (D) Selected genes for the main cell populations identified in C.

Supporting image 3

Fig. 3: Stromal cell signalling in SjD. (A) Non-immune cell type proportions in 3 independent donors, inferred from scRNA-seq data (Fig. 2A). (B) Difference between number of predicted interactions found in early and late donors for each cell type pair. Cell types in rows represent those emitting ligands; cell types in columns are those with the target receptor. (C) H&E staining of salivary glands of a late donor. Inset shows representative immune cell infiltrate. (D) Expression of CCL19 (ligand) and CCR7 (receptor) in spatial transcriptomics data of the gland shown in C.


Disclosures: T. Gomes: None; M. Bandeira: None; R. do Amaral Vieira: None; B. Correia: None; S. Barreira: None; P. Gaspar: None; R. Cruz-Machado: None; B. Filipe: None; P. Ávila-Ribeiro: None; F. Ribeiro: None; B. Vidal: None; B. Val: None; F. Costa: None; A. Teodósio Chícharo: None; A. Silva: None; M. Silvério-Antonio: None; J. Forjaz Lacerda: None; J. Eurico Fonseca: None; D. López Presa: None; N. Khmelinskii: None; S. Kumar: None; L. Graca: None; V. C. Romão: None.

To cite this abstract in AMA style:

Gomes T, Bandeira M, do Amaral Vieira R, Correia B, Barreira S, Gaspar P, Cruz-Machado R, Filipe B, Ávila-Ribeiro P, Ribeiro F, Vidal B, Val B, Costa F, Teodósio Chícharo A, Silva A, Silvério-Antonio M, Forjaz Lacerda J, Eurico Fonseca J, López Presa D, Khmelinskii N, Kumar S, Graca L, C. Romão V. Unraveling the Progression of Sjögren’s Disease at the Cellular and Histological Level Using Single-cell and Spatial Transcriptomics [abstract]. Arthritis Rheumatol. 2024; 76 (suppl 9). https://acrabstracts.org/abstract/unraveling-the-progression-of-sjogrens-disease-at-the-cellular-and-histological-level-using-single-cell-and-spatial-transcriptomics/. Accessed .
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