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Induction of Experimental Autoimmune Hypophysitis in SJL Mice
Published on: December 17, 2010
Aged Sanroque Mice Spontaneously Develop Sjögren's Syndrome-like Disease
Suk San Choi1, Eunkyeong Jang1, Yeon-Kyung Oh1
1Laboratory of Autoimmunology, Department of Anatomy and Cell Biology, Hanyang University College of Medicine, Seoul 04763, Korea.
Immune Network
|March 7, 2019
Summary
Sjögren's syndrome (SS) development in lupus-prone mice is linked to follicular helper T (Tfh) cell dysregulation. Chronic Tfh cell issues in specific lymph nodes drive SS pathogenesis, offering insights into autoimmune disease mechanisms.
Area of Science:
- Immunology
- Autoimmune Diseases
- Rheumatology
Background:
- Sjögren's syndrome (SS) is a chronic autoimmune disorder primarily affecting salivary and lacrimal glands, with unknown etiology.
- Co-occurrence of SS and lupus suggests shared pathogenic pathways.
- The lupus-prone sanroque (SAN) mouse strain provides a model to investigate shared autoimmune mechanisms.
Purpose of the Study:
- To determine if SS develops in the lupus-prone SAN mouse model.
- To investigate the role of follicular helper T (Tfh) cells in SS pathogenesis within this model.
Main Methods:
- Female SAN mice were monitored for SS-like symptoms.
- Saliva flow rate, sialadenitis, and IgG deposits in salivary glands were assessed.
- Serum autoantibody titers and autoantibody-secreting cells in cervical lymph nodes (LNs) were quantified.
- Tfh cell populations in LNs were analyzed.
Main Results:
- Female SAN mice developed lupus-like symptoms around 20 weeks of age.
- SS-typical manifestations, including reduced saliva flow and sialadenitis, appeared around 40 weeks of age.
- Elevated SS-related autoantibodies and increased autoantibody-secreting cells in cervical LNs preceded SS pathology.
- Expansion of Tfh cells and effector cells correlated with SS development.
Conclusions:
- Chronic dysregulation of Tfh cells in salivary gland-draining LNs is sufficient to induce SS in lupus-prone mice.
- This study highlights a potential common mechanism in the pathogenesis of SS and lupus.
- Findings provide a framework for understanding SS etiology and developing targeted therapies.
