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Induction of intercellular adhesion molecule-1 but not of lymphocyte function-associated antigen-3 in thyroid
1Immunology Unit, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Spain.
Insights
Cytokines like IFN-gamma, IL-1 beta, and TNF-alpha enhance intercellular adhesion molecule-1 (ICAM-1) expression on thyrocytes, suggesting a role in thyroid autoimmune diseases. Lymphocyte function-associated antigen-3 (LFA-3) expression remained unaffected.
Area of Science:
- Immunology
- Endocrinology
- Cell Biology
Background:
- Thyrocytes, the cells of the thyroid gland, play a crucial role in hormone production.
- Understanding their immune interactions is vital for comprehending thyroid autoimmune diseases.
Purpose of the Study:
- To investigate the expression of ICAM-1 and LFA-3 on thyrocytes.
- To determine how cytokines regulate the expression of these molecules.
- To assess the potential role of thyrocyte immune molecule expression in thyroid autoimmunity.
Main Methods:
- Immunofluorescence studies on cryostat sections and dispersed thyrocytes.
- Culture of normal thyrocytes and the HT93 thyroid cell line.
- Treatment with cytokines: IFN-gamma, IL-1 beta, and TNF-alpha.
Main Results:
- ICAM-1 and LFA-3 were minimally expressed on normal thyrocytes but induced by cytokines.
- IFN-gamma, IL-1 beta, and TNF-alpha significantly enhanced ICAM-1 expression.
- LFA-3 expression was not modulated by the tested cytokines.
- The HT93 thyroid cell line showed constitutive high expression of ICAM-1 and LFA-3, with ICAM-1 further modulated by cytokines.
Conclusions:
- Normal thyrocytes are largely immunologically silent.
- Cytokine-induced ICAM-1 expression on thyrocytes, alongside HLA molecules, suggests they can participate in antigen presentation.
- These findings support the hypothesis that thyrocytes can be recognized as target cells in autoimmune thyroid diseases.
Abstract:
We investigated the expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-3 (LFA-3) by thyrocytes and their regulation by cytokines. Immunofluorescence studies on cryostat sections and on freshly dispersed cell preparations showed that ICAM-1 and LFA-3 are barely detectable in non-autoimmune thyrocytes. However, thyrocytes acquired ICAM-1 expression in culture. IFN-gamma, IL-1 beta and TNF-alpha produced a clear enhancement of ICAM-1 expression. When tested in combination, IL-1 beta and TNF-alpha were additive to the IFN-gamma effect. LFA-3 expression was not modulated by these cytokines. In the HT93 thyroid cell line generated by transfection with SV40, ICAM-1 and LFA-3 were both constitutively expressed at high levels. Cytokines modulated ICAM-1 expression similarly, but to a greater extent than in normal thyrocytes. LFA-3 remained unmodified. These results support the notion that normal thyrocytes are immunologically silent cells. The capability of cytokines to induce ICAM-1 together with HLA class I and class II-expression on thyrocytes suggests that under their influence, these cells may express all the surface molecules required for antigen presentation and/or for being recognized as target cells in the context of thyroid autoimmune disease.