Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA146907 | ENA |
REPOSITORIES: ENA
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Project description:NOD mice were injected once a week with LTBR-Ig to block the LTBR-pathway, or with control monoclonal antibody MOPC from age 8 to 16 weeks old. Extraorbital lacrimal glands or submaxillary glands were dissected and total mRNA prepared. Each sample was either the combined lacrimals (2) from each mouse or individual salivary glands. There were 4 mice in each treatment group. Total mRNA was isolated and the quality was assessed using the Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA). Reverse transcription to prepare cDNA was performed using Invitrogen M-MLV system. The purpose was to determine changes in gene expression in glands due to blockade of the LTBR-pathway. Differential Gene Expression in NOD mouse lacrimal and salivary glands after LTBR-Ig treatment
2011-10-06 | E-GEOD-32681 | biostudies-arrayexpress
Project description:NOD mice were injected once a week with LTBR-Ig to block the LTBR-pathway, or with control monoclonal antibody MOPC from age 8 to 16 weeks old. Extraorbital lacrimal glands or submaxillary glands were dissected and total mRNA prepared. Each sample was either the combined lacrimals (2) from each mouse or individual salivary glands. There were 4 mice in each treatment group. Total mRNA was isolated and the quality was assessed using the Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA). Reverse transcription to prepare cDNA was performed using Invitrogen M-MLV system. The purpose was to determine changes in gene expression in glands due to blockade of the LTBR-pathway.
2011-10-07 | GSE32681 | GEO
Project description:NOD mice spontaneously develop lacrimal gland inflammation. NOD mice that lack TLR7 or that lack IFNAR1 are protected from developing lacrimal gland inflammation. RNA sequencing studies were performed to compare gene expression profiles in lacrimal glands from wild-type (WT) vs Tlr7 knockout or Ifnar1 knockout nonobese diabetic (NOD) mice to determine disease-relevant gene and pathway profiles upregulated in WT lacrimal glands in either a TLR7- or IFNAR1-dependent manner.
2021-01-04 | GSE161184 | GEO
Project description:Purpose: Sjögren's syndrome (SS) is a group of chronic autoimmune diseases primarily targeting exocrine glands, including the lacrimal glands (LG). Involvement of the lacrimal glands leads to severe dry eye, also known as Sjögren’s syndrome-associated dry eye (SSDE). Current, available animal models of SS are achieved by using autoantigens from salivary gland. This study aims to establish a SSDE mouse model using lacrimal glands as autoantigen. Methods: To establish the LGSS model, autoimmune responses were induced in mice using homogenized lacrimal gland proteins. LGSS mice were evaluated at various timepoints after immunization to determine SS development. SS phenotype such as tear and saliva secretion, lymphocyte infiltration in the lacrimal and salivary glands and serum autoantibody levels was assessed. Immune cell profiles in the spleen and cervical lymph nodes were evaluated via flow cytometry. In addition, corneal epithelial intactness, goblet cell density, lacrimal gland injury were evaluated to assess lacrimal gland involvement and secondary ocular surface damage. RNA sequencing and gene enrichment analysis of diseased lacrimal glands were performed. Results: LGSS mice demonstrated a reduced tear and saliva secretion, increased lymphocyte infiltration, and elevated autoantibody levels that are similar to common SS mice. Additionally, the established LGSS mice demonstrated increased populations of Th1 and Th17 cell, along with lacrimal gland and ocular surface damage. RNA sequencing revealed that LGSS mice shared a common genetic profile with NOD mice, the spontaneous SS model, such as Parp9, Cdkn2c, and Ifi35. Additionally, LGSS mice exhibited several uniquely expressed genes, including metabolism-related genes (Cbs, Dlst, Sardh) and genes associated with cellular processes (Actc1, Tnnc1). Conclusion: The LGSS mice have been shown that successfully replicates several key features of SS and demonstrates significant lacrimal gland and ocular surface damages, making it a valuable animal model to study SSDE.
2025-12-25 | GSE285438 | GEO
Project description:Prior to the onset of autoimmune destruction, type 1 diabetic patients and an animal model thereof, the nonobese diabetic (NOD) mouse, show morphological and functional abnormalities in target organs, which may act as inciting events for leukocyte infiltration. To better understand these abnormalities, but without the complications associated with inflammatory infiltrates, we examined genes expressed in autoimmune target tissues (pancreas, submandibular glands, and lacrimal glands) of NOD/scid mice and of autoimmune-resistant C57BL6/scid mice. Experiment Overall Design: Pancreata (6 weeks old mice), submandibular (9 and 15 weeks), and lacrimal glands (15 weeks) from individual NOD-scid and B6-scid mice were isolated for RNA extraction and hybridization on Affymetrix microarrays.
2007-11-29 | E-GEOD-4953 | biostudies-arrayexpress
Project description:Sjögren's disease (SjD) is an autoimmune condition characterized by the dysfunction of the salivary and lacrimal glands. The study aimed to decipher the pathogenic cell populations and their immunological pathways in the salivary glands. We further determined the therapeutic effect of inhibiting DOCK2 shared by novel clusters of CD8Cd8+ T cells in a SjD mouse model.
2024-12-19 | GSE268532 | GEO
Project description:Primary Sjögren’s syndrome (pSS) is a systemic autoimmune disease characterized by reduced activity of the exocrine glands (principally the salivary and lacrimal glands) due to chronic lymphocytic infiltration. pSS has been closely associated with an enhanced risk of mucosa-associated lymphoid tissue (MALT) lymphoma. However, the dynamic epigenetic changes in gland cells accompanied with this pathogenesis are not fully understood. In present study, the labial gland (LG) and parotid gland (PG) tissues from two pSS patients with lymphoma were harvested including LG with negative antinuclear antibodies (ANA) and LG with positive ANA at the first diagnosis of pSS, as well as PG with and without lymphoma tissues at the second diagnosis of MALT. RNA-seq of these tissues were studied. This data is benefit to advanced understanding the dynamic development of MALT from pSS, emphasizing the importance of epigenetic alterations in regulating transcription during the pathologic process.
2021-04-17 | E-MTAB-10339 | biostudies-arrayexpress
Project description:Transcriptome analysis of submandibular glands in female MyD88+/+ and MyD88−/− NOD mice. Sjögren's syndrome (SS) is an autoimmune disease characterized by dysfunction of salivary glands (SGs) and lacrimal glands, which is caused by chronic inflammation associated with autoantibody and autoreactive lymphocyte infiltration. The pathogenic mechanism of SS has not been fully elucidated. Infiltrated lymphocytes form regularized structures similar to lymphoid follicles of secondary lymphoid organs, such as T/B cell compartments, high endothelial venules (HEVs), lymphatic vessels, and germinal centers, therefore being believed as an ectopic lymphoid tissue called tertiary lymphoid organs (TLO). We previously found that deletion of the Toll-like receptor/IL-1 receptor (TLR/IL-1R) adaptor molecule gene Myd88 in SS model mice NOD reduced the frequency of lymphocyte infiltration and HEV formation in SGs. In this study, we analyzed the effect of MyD88 deficiency on lymphoid follicle formation in SGs of NOD mice. Microarray analysis showed decreased expression of genes related to TLO, such as Cxcl13 and Cxcr5, in Myd88-deficient SGs. These results indicate that deficiency of TLR/IL-1R signaling decrease gene expression ot chemokines in SGs, suggesting MyD88-dependent signaling is directly involved in formation of lymphoid follicles in SS.
2021-09-01 | GSE157669 | GEO
Project description:Primary Sjögren’s syndrome (pSS) is a systemic autoimmune disease characterized by reduced activity of the exocrine glands (principally the salivary and lacrimal glands) due to chronic lymphocytic infiltration. pSS has been closely associated with an enhanced risk of mucosa-associated lymphoid tissue (MALT) lymphoma. However, the dynamic epigenetic changes in gland cells accompanied with this pathogenesis are not fully understood. In present study, the labial gland (LG) and parotid gland (PG) tissues from two pSS patients with lymphoma were harvested including LG with negative anti-SSA/SSB and LG with positive anti-SSA/SSB at the first diagnosis of pSS, as well as PG with and without lymphoma tissues at the second diagnosis of MALT. ChIP-seq of H3K4/9/27/36/79me3 were performed. This data is benefit to advanced understanding the dynamic development of MALT from pSS, emphasizing the importance of epigenetic alterations in regulating transcription during the pathologic process.
2021-04-17 | E-MTAB-10340 | biostudies-arrayexpress
Project description:Primary Sjögren’s syndrome (pSS) is an autoimmune disease characterized by inflammation and damage to exocrine glands, leading to symptoms such as dry eye and reduced tear production. The NF-κB signaling pathway plays a critical role in the inflammatory processes underlying pSS. The aims of the present in vivo study were to investigate the role of NF-κB signaling in lacrimal gland damage and tear secretion in the NOD/Ltj mouse, and to explore the therapeutic potential of NF-κB inhibition. The animal model was established using NOD/Ltj mouse and lacrimal gland pathological change was showed by H&E. Bioinformatics analysis was conducted through RNA sequencing (RNA-seq) and confirmed by RT-qPCR and Western blot. The NOD/Ltj mouse were treated with NF-κB inhibitor JSH-23. Tear secretion assays, ELISA, TUNEL staining, immunofluorescence, immunohistochemistry, and flow cytometry were employed to assess the role of NF-κB signaling in tear production, inflammatory cytokine expression, cell apoptosis, differentially expressed genes (DEGs), and cell differentiation in lacrimal gland damage in pSS mouse. NF-κB signaling was significantly activated in NOD/Ltj mouse lacrimal gland and pSS-related dry eye. NF-κB blockage decreased cell apoptosis, reduced inflammatory cytokine expression, and inhibited Th17 cell differentiation in NOD/Ltj mouse lacrimal glands, as well as restored tear production and normalized the expression of DEGs CARD14 and CCL19. NF-κB signaling played a pivotal role in lacrimal gland damage in pSS model NOD/Ltj mouse by involvement of cell apoptosis, inflammatory cytokine expression and Th17 cell differentiation. Targeting NF-κB signaling may offer a promising therapeutic approach for managing pSS-related dry eye.
2025-08-25 | GSE306385 | GEO