Gene Expression Profiling of Lacrimal Glands Identifies the Ectopic Expression of MHC II on Glandular Cells as a Presymptomatic Feature in a Mouse Model of Primary Sjögren's Syndrome

@article{Yin2018GeneEP,
  title={Gene Expression Profiling of Lacrimal Glands Identifies the Ectopic Expression of MHC II on Glandular Cells as a Presymptomatic Feature in a Mouse Model of Primary Sj{\"o}gren's Syndrome},
  author={Junping Yin and Junfeng Zheng and Fengyuan Deng and Wenjie Zhao and Yan Chen and Qiaoniang Huang and Renliang Huang and Lifang Wen and Xiaoyang Yue and Frank Petersen and Xinhua Yu},
  journal={Frontiers in Immunology},
  year={2018},
  volume={9}
}
Ectopic expression of MHC II molecules on glandular cells is a feature of primary Sjögren's syndrome (pSS). However, the cause of this ectopic expression and its potential role in the pathogenesis of the disease remains elusive. Here, we report that ectopic expression of MHC II molecules on glandular cells represents an early presymptomatic event in a mouse model of pSS induced by immunization of Ro60_316-335 peptide emulsified in TiterMax® as an adjuvant. Ectopic expression of MHC II was… 

Figures from this paper

Recent Advances in Mouse Models of Sjögren's Syndrome
TLDR
This review aims to provide a comprehensive overview of recent advances in the field of experimental Sjögren's syndrome by reviewing mouse models, genetic models, and induced models, in which mice spontaneously develop SS-like disease.
Serum Levels of Autoantibodies Against Extracellular Antigens and Neutrophil Granule Proteins Increase in Patients with COPD Compared to Non-COPD Smokers
  • A. Ma, Lifang Wen, Xinhua Yu
  • Medicine, Biology
    International journal of chronic obstructive pulmonary disease
  • 2020
TLDR
The comprehensiveAutoantibody profiles from COPD patients established in this study demonstrated for the first time a shift in the cellular localization of antigens targeted by autoantibodies in COPD.
COPD_A_235903 189..200
Aiping Ma,* Lifang Wen,* Junping Yin, Yi Hu, Xiaoyang Yue, Jiurong Li, Xiaoru Dong, Yask Gupta, 5 Ralf J Ludwig, 5 Susanne Krauss-Etschmann, 3,6 Gabriela Riemekasten, Frank Petersen, Xinhua Yu 2,3

References

SHOWING 1-10 OF 33 REFERENCES
Expression of the retinoblastoma protein RbAp48 in exocrine glands leads to Sjögren's syndrome–like autoimmune exocrinopathy
TLDR
It is reported that transgenic (Tg) expression of RbAp48 resulted in the development of autoimmune exocrinopathy resembling Sjögren's syndrome, indicating a novel immunocompetent role of epithelial cells that can produce IFN-γ, resulting in loss of local tolerance before developing gender-based autoimmunity.
Possible function of salivary gland epithelial cells as nonprofessional antigen-presenting cells in the development of Sjögren's syndrome.
TLDR
The ability of salivary gland epithelial cells to express HLA-DR antigens, costimulatory molecules, and adhesion molecules and thus to act as nonprofessional APC was suggested.
B Cells Are Indispensable for a Novel Mouse Model of Primary Sjögren’s Syndrome
TLDR
A novel mouse model for primary Sjögren’s syndrome is provided and an indispensable role of B cells is revealed in this model and it suggests that T cell epitope within Ro60 antigen is potentially pathogenic for pSS.
Lack of Apoptosis of Infiltrating Cells as the Mechanism of High Susceptibility to EAE in DA Rats
TLDR
It is postulate that in addition to higher IFN-γ and TNF-α production, resistance to early apoptosis of the invading cells in the target tissue possibly due to lack of downregulation by TGF-β leads to exceptional susceptibility to EAE in DA rats.
Transfer of human serum IgG to nonobese diabetic Igmu null mice reveals a role for autoantibodies in the loss of secretory function of exocrine tissues in Sjögren's syndrome.
TLDR
Findings indicate that autoantibodies play an important part in the functional impairment of secretory processes seen in connection with the autoimmune exocrinopathy of Sjögren's syndrome.
Early pathogenic events associated with Sjögren's syndrome (SjS)-like disease of the nod mouse using microarray analysis
TLDR
Altered gene expressions of TLR3 and TNF-superfamily-receptors and ligands during this early phase of SjS suggest a possible viral etiology in the altered glandular homeostasis with an upregulated, possibly overstimulated, B-lymphocyte activation in the early autoimmune response present in the submandibular glands.
Epithelial HLA-DR expression and T lymphocyte subsets in salivary glands in Sjögren's syndrome.
TLDR
Salivary glands obtained at biopsy from patients with Sjögren's syndrome and controls were studied with regard to phenotype of infiltrating and residing cells, by means of a double immunoenzymatic staining technique, to indicate the induction of HLA-DR expression in nonlymphocytic cells of target organs.
Overexpression of phosphorylated STAT-1alpha in the labial salivary glands of patients with Sjögren's syndrome.
TLDR
Evidence is found of the up-regulation of STAT-1alpha mRNA and protein in LSGs from SS patients, as well as the presence of pSTAT-1 alpha in ductal epithelium fromSS patients.
Sjögren's Syndrome‐Like Disease of C57BL/6.NOD‐Aec1 Aec2 Mice: Gender Differences in Keratoconjunctivitis Sicca Defined by a Cross‐Over in the Chromosome 3 Aec1 Locus
TLDR
It is suggested that SjS‐like disease in the NOD mouse shows gender‐specific regulation determined by autosomal genes, whereas female mice exhibit stomatitis sicca in the absence of detectable keratoconjunctivitis sICca.
...
...