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Apoptosis and the thymic microenvironment in murine lupus
Y Takeoka1, N Taguchi, L Shultz
1Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, School of Medicine, Davis, California 95616, USA.
Journal of Autoimmunity
|November 7, 1999
Summary
Murine lupus models show significant thymic abnormalities, including reduced apoptosis and altered architecture. These thymic microenvironment changes are crucial in the development of lupus.
Area of Science:
- Immunology
- Pathology
- Developmental Biology
Background:
- The thymus in New Zealand black (NZB) mice exhibits premature involution and thymic epithelial cell degeneration.
- NZB mice display unique thymic stromal cell abnormalities, detectable with specific monoclonal antibodies.
- Thymic architecture and apoptosis are critical for immune system development and self-tolerance.
Purpose of the Study:
- To investigate apoptosis induction and thymic epithelial architecture changes in murine lupus models.
- To analyze the role of the thymic microenvironment in the pathogenesis of lupus.
- To compare apoptosis susceptibility in different lupus strains versus control mice.
Main Methods:
- Studied apoptosis in NZB, MRL/lpr, BXSB/Yaa, C3H/gld mice, and BALB/c, C57BL/6 controls.
- Assessed basal and induced apoptosis (dexamethasone, lipopolysaccharide [LPS]) in thymocytes.
- Utilized monoclonal antibodies to examine thymic stromal architecture and thymic nurse cells (TNCs).
Main Results:
- Apoptosis was predominantly in the thymic cortex; lupus models showed <20% of control apoptosis frequency.
- All lupus strains exhibited severe cortical network abnormalities.
- Murine lupus thymus was less susceptible to LPS-induced apoptosis; NZB mice had the lowest TNC count.
Conclusions:
- Significant abnormalities in apoptosis induction and TNC-like cell formation occur in lupus models.
- Thymic microenvironment alterations play a key role in the pathogenesis of murine lupus.
- These findings highlight the thymus's importance in lupus development and progression.