Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA146907 | ENA |
REPOSITORIES: ENA
Similar Datasets
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: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: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: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: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:To identify the transcriptomic alterations within the different cellular compartments of the lacrimal gland during chronic inflammation, we analyzed the lacrimal glands of NOD.B10.H2b vs BALB/cJ with 10X Visium technology
2022-09-23 | GSE210380 | GEO
Project description:Sjögren's Syndrome (SS) is an autoimmune exocrinopathy characterized by the progressive damage of salivary and lacrimal glands associated with lymphocytic infiltration. It can be defined as primary SS (pSS) or associated/secondary SS (sSS) if combined with another systemic autoimmune disease. Identifying new non-invasive biomarkers for SS diagnosis remains a challenge, and alterations in saliva composition reported in patients turn this fluid into a source of potential biomarkers. To examine the overall panorama of proteins in saliva, samples of control, pSS, and sSS individuals were analyzed by gel-based LC-MS/MS.
2021-06-09 | PXD025463 | Pride
Project description:Sjögren's Syndrome (SS) is an autoimmune exocrinopathy characterized by the progressive damage of salivary and lacrimal glands associated with lymphocytic infiltration. It can be defined as primary SS (pSS) or associated/secondary SS (sSS) if combined with another systemic autoimmune disease. Identifying new non-invasive biomarkers for SS diagnosis remains a challenge, and alterations in saliva composition reported in patients turn this fluid into a source of potential biomarkers. To examine the overall panorama of proteins in saliva, samples of control, pSS, and sSS individuals were analyzed by gel-free LC-MS/MS.
2021-06-09 | PXD025434 | Pride