Abstract
Immune thrombocytopenia is an autoimmune disease with abnormal T cell immunity. Cytotoxic T cells, abnormal T regulatory cells, helper T cell imbalance, megakaryocyte maturation abnormalities and abnormal T cell anergy are involved in the pathogenesis of this condition. The loss of T cell-mediated immune tolerance to platelet auto-antigens plays a crucial role in immune thrombocytopenia. The induction of T cell tolerance is an important mechanism by which the pathogenesis and treatment of immune thrombocytopenia can be studied. Studies regarding the roles of the new inducible costimulator signal transduction pathway, the ubiquitin proteasome pathway, and the nuclear factor kappa B signal transduction pathway in the induction of T cell tolerance can help improve our understanding of immune theory and may provide a new theoretical basis for studying the pathogenesis and treatment of immune thrombocytopenia.
Highlights
Immune thrombocytopenia (ITP), known as idiopathic thrombocytopenic purpura, is an immune-mediated disease of adults and children that is characterized by excessive platelet destruction and decreased platelet production
Indirubin injection significantly increases the inhibitory function of T regulatory cells (Tregs) cells. These findings suggest that indirubin promotes immune tolerance in ITP [22]
Inhibition of the ubiquitin proteasome pathway Blocking the major histocompatibility complex (MHC) class I antigen processing, presentation, and nuclear factor kappa B (NF-κB) signal transduction system can inhibit the proliferation of lymphocyte activation and induce ITP T cell tolerance
Summary
Immune thrombocytopenia (ITP), known as idiopathic thrombocytopenic purpura, is an immune-mediated disease of adults and children that is characterized by excessive platelet destruction and decreased platelet production. New co-stimulatory signal pathway-inducible co-stimulator (ICOS) pathway Blocking ICOS co-stimulation pathways to inhibit the activity of ITP T cells in immune tolerance induction provides a theoretical basis for the mechanism and treatment of ITP. Inhibition of the ubiquitin proteasome pathway Blocking the MHC class I antigen processing, presentation, and nuclear factor kappa B (NF-κB) signal transduction system can inhibit the proliferation of lymphocyte activation and induce ITP T cell tolerance. These observations may help identify new ways to achieve artificial immune tolerance induced by the proteasome system. This finding provides a theoretical basis for inducing ITP T cell tolerance by blocking the proteasome pathway and the NF-κB signaling pathway
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
