Related Experiment Videos
Expression and function of membrane attack complex inhibitory proteins on thyroid follicular cells
N Tandon1, B P Morgan, A P Weetman
1Department of Medicine, University of Sheffield Clinical Sciences Centre, Northern General Hospital, U.K.
Immunology
|February 1, 1992
Summary
Human thyroid cells resist complement attack via CD59 antigen and MIP/HRF proteins. Cytokines boost these inhibitors, enhancing thyroid cell resistance to lysis in autoimmune thyroid disease.
Area of Science:
- Immunology
- Cell Biology
- Endocrinology
Background:
- Human thyroid cells exhibit resistance to lysis mediated by the homologous membrane attack complex.
- Autoimmune thyroid diseases like Graves' disease and Hashimoto's thyroiditis involve complex immune responses affecting thyroid function.
Purpose of the Study:
- To investigate the role of membrane attack complex (MAC)-inhibiting proteins in human thyroid cells.
- To determine the impact of cytokines on MAC inhibitor expression and thyroid cell susceptibility to complement-mediated lysis.
Main Methods:
- Immunohistochemical staining was used to detect CD59 antigen and membrane attack complex-inhibiting protein/homologous restriction factor (MIP/HRF) expression in thyroid tissues.
- In vitro experiments involved treating thyroid cells with interleukin-1 (IL-1), tumor necrosis factor (TNF), and interferon-gamma (IFN-γ).
- Blocking experiments utilized monoclonal antibodies against CD59 antigen and MIP/HRF to assess their contribution to complement resistance.
Main Results:
- Normal thyroid cells and those in Graves' disease and Hashimoto's thyroiditis express both CD59 antigen and MIP/HRF.
- Cytokine treatment (IL-1, TNF, IFN-γ) enhanced the expression of both inhibitors, leading to increased resistance of thyroid cells to complement-mediated lysis.
- Blocking studies indicated that both CD59 antigen and MIP/HRF contribute to resistance, with CD59 antigen playing a more significant role.
Conclusions:
- CD59 antigen and MIP/HRF are key proteins conferring resistance to homologous complement attack in human thyroid cells.
- Cytokine-induced upregulation of these inhibitors influences thyroid cell survival in inflammatory conditions.
- The expression levels of CD59 antigen and MIP/HRF may determine the extent of tissue damage in autoimmune thyroid diseases driven by complement-fixing antibodies.