Cyclosporin A-induced autoimmunity: the result of defective de novo T-cell development
Language English Country Czech Republic Media print
Document type Journal Article, Review
PubMed
10730868
Knihovny.cz E-resources
- MeSH
- Autoimmunity drug effects radiation effects MeSH
- Autoimmune Diseases etiology immunology pathology MeSH
- Models, Biological MeSH
- Cell Differentiation drug effects MeSH
- Cyclosporine adverse effects MeSH
- Immunosuppressive Agents adverse effects MeSH
- Humans MeSH
- T-Lymphocyte Subsets cytology drug effects immunology MeSH
- Thymus Gland cytology drug effects immunology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- Cyclosporine MeSH
- Immunosuppressive Agents MeSH
Cyclosporin A-induced autoimmunity (CsA-AI) is an autoimmune disease, caused by the combinatory treatment with irradiation and cyclosporin A (CsA). CsA-AI is the result of defective T-cell maturation leading to disturbed T-cell balances in the periphery. Increases in Th1 cells and reduction of autoregulatory cells eventually enable the enumerated autoreactive CD4 and CD8 T cells to disturb the homeostasis in the target organs. In unravelling the effect of CsA on T-cell maturation and the role of T cells in CsA-AI many pieces have been put in their places; nevertheless, some remain the topic of debate. The identity of the autoantigen(s) remains elusive, the working mechanism of the autoregulatory cells still is to be determined, and the interplay between CD4 and CD8 T-cell subsets in relation to type-1 and type-2 responses is a matter of interest. In spite of all these unknowns, the CsA-AI autoimmune model is, in contrast to many autoimmune models induced by immunization with a foreign protein in adjuvant, an interesting physiological model based on defective T-cell development including aberrant selection in the thymus and disturbed T-cell balances in the periphery.