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Spontaneous autoimmune dacryoadenitis in aged CD25KO mice.

Ehsan Rahimy1, John D Pitcher, Solherny B Pangelinan

  • 1Ocular Surface Center, Cullen Eye Institute, Baylor College of Medicine, Houston, TX 77030, USA.

The American Journal of Pathology
|June 23, 2010
PubMed
Summary

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Mice lacking CD25 (CD25KO) showed early autoimmune infiltration and dysfunction in lacrimal glands, with a shift from Th-17 to Th-1 inflammation over time.

Area of Science:

  • Immunology
  • Ophthalmology
  • Autoimmunity

Background:

  • The lacrimal glands (LGs) are crucial for maintaining ocular surface health.
  • Dysfunction of LGs leads to dry eye disease, a condition with significant clinical impact.
  • Understanding the immunopathogenesis of LG dysfunction is vital for developing targeted therapies.

Purpose of the Study:

  • To investigate the time-related immunopathological changes in the lacrimal glands (LGs) of CD25 knockout (CD25KO) mice.
  • To assess the impact of these changes on LG function and identify key inflammatory pathways involved.

Main Methods:

  • Comparative analysis of LGs from C57BL/6 (wild-type) and CD25KO mice at 8, 12, and 16 weeks of age.
  • Quantification of T cell infiltration (CD4, CD8) via flow cytometry.

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  • Assessment of LG function through tear peroxidase activity and epidermal growth factor (EGF) mRNA expression.
  • Evaluation of T helper (Th)-1, -2, and -17 cytokine expression using real-time PCR.
  • Analysis of epithelial apoptosis using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and activated caspase-3 staining.

    • Main Results:

    • CD25KO mice exhibited significant CD4 and CD8 T cell infiltration in LGs starting at 8 weeks, peaking at 12 weeks.
    • Complete loss of peroxidase secretion and minimal EGF mRNA expression were observed in CD25KO mice.
    • Ductal epithelial apoptosis was evident in CD25KO mice.
    • Young CD25KO LGs showed elevated Th-17 and Th-1 associated cytokine transcripts compared to wild-type.
    • A time-related decrease in IL-17A and CCL20 was observed in CD25KO LGs, alongside a shift towards Th-1 inflammation.

    Conclusions:

    • Autoimmune infiltration and functional loss of lacrimal glands occur early (by 8 weeks) in CD25KO mice.
    • A temporal shift from Th-17 to Th-1 mediated inflammation characterizes the immunopathology in CD25KO mouse LGs.
    • These findings highlight the critical role of CD25 in regulating immune responses within the lacrimal glands and preventing autoimmune-mediated dysfunction.