T cell receptor V beta usage in murine experimental autoimmune thyroiditis

Area of Science:

• Immunology
• Autoimmunity
• Endocrinology

Background:

• Experimental autoimmune thyroiditis (EAT) is an animal model for autoimmune thyroid disease.
• EAT can manifest in lymphocytic or granulomatous forms, both primarily driven by CD4+ T cells.
• Understanding the T cell receptor (TCR) repertoire involved is crucial for elucidating EAT pathogenesis.

Purpose of the Study:

• To investigate the specific T cell receptor (TCR) V beta families present in the thyroid infiltrate during experimental autoimmune thyroiditis (EAT).
• To compare TCR V beta usage between lymphocytic and granulomatous forms of EAT.
• To assess the role of specific V beta families in EAT severity.

Main Methods:

• Induction of EAT in mice using mouse thyroglobulin (MTg)-sensitized spleen cells.
• Analysis of thyroid infiltrates using flow cytometry and reverse transcription-polymerase chain reaction (RT-PCR).
• Depletion of specific T cell populations (V beta 8+) to evaluate their role in disease.

Main Results:

• Flow cytometry identified V beta 8, V beta 4, V beta 11, and V beta 14 as predominant TCRs in the thyroid infiltrate.
• RT-PCR confirmed these and detected additional V beta families, with no significant differences between lymphocytic and granulomatous EAT.
• TCR V beta usage shifted over time, and depletion of V beta 8+ T cells did not alter EAT severity, indicating a broader TCR involvement.

Conclusions:

• Multiple T cell receptor (TCR) V beta families are expressed in the thyroids of mice with experimental autoimmune thyroiditis (EAT).
• The TCR repertoire in EAT is diverse and involves multiple V beta gene families.
• Further research is needed to fully understand the contribution of different TCRs to EAT pathogenesis.