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Induction of experimental autoimmune thyroiditis in B cell-depleted mice
L S Rayfield1, T A Smith, S J Andrews
1Department of Immunology, United Medical School, Guy's Hospital, London Bridge, U.K.
Immunology Letters
|January 15, 1989
Summary
B cell depletion did not prevent experimental autoimmune thyroiditis induction in mice. However, B cells may contribute to increased disease severity in this autoimmune thyroid condition.
Area of Science:
- Immunology
- Endocrinology
- Autoimmunity
Background:
- Experimental autoimmune thyroiditis (EAT) is a model for autoimmune thyroid disease.
- The role of B cells in the induction and severity of EAT requires further elucidation.
Purpose of the Study:
- To investigate the effect of B cell depletion on the induction and severity of murine EAT.
- To determine if autoantibodies are essential for EAT development.
Main Methods:
- CBA mice were treated with rabbit anti-mouse Ig antibody for B cell depletion.
- Controls received normal rabbit IgG or no injection.
- EAT was induced using murine thyroid extract in complete Freund's adjuvant.
- B cell deficiency was confirmed by serum IgM, spleen cell immunofluorescence, and LPS responsiveness.
Main Results:
- Thyroiditis was induced in mice despite B cell depletion.
- A significant proportion of B cell-depleted mice exhibited low levels of anti-thyroglobulin autoantibodies.
- B cell depletion did not completely abrogate EAT induction.
Conclusions:
- Autoimmune thyroiditis can be induced in the absence of B cells and significant autoantibody production.
- B cells may play a role in exacerbating the severity of experimental autoimmune thyroiditis.