Cytotoxic T cells react to cardiac peptides in patients with cancer that receive immunotherapy, resulting in myocarditis. Identifying the targets for T cells in patients who are immunosuppressed will enable a better understanding of individual risk before treatment is initiated.
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| http://dx.doi.org/10.1038/s44161-022-00184-9 | DOI Listing |
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Autoimmune effector mechanisms associated with a defective immunosuppressive axis in immune thrombocytopenia (ITP).
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Division of Hematology and Transfusion Medicine, Lund University, Lund, Sweden; Clinical Immunology and Transfusion Medicine, Office of Medical Services, Region Skåne, Lund, Sweden; Departments of Pharmacology, Medicine and Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada. Electronic address:
Article Synopsis
- Immune thrombocytopenia (ITP) is an autoimmune disorder marked by low platelet counts, with varying symptoms ranging from no bleeding to severe, potentially fatal bleeding.
- The disease involves a malfunction in the immune system, particularly a hyperactive response from certain immune cells that destroy platelets and their precursors.
- Key factors in this condition include a breakdown of immune regulation, characterized by defects in certain immunosuppressive cells, leading to an uncontrolled immune response that attacks platelets and disrupts their production.
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Autoimmune diseases are characterized by overactive immunity, where the body's defense system launches an attack against itself. If left unchecked, this can result in the destruction of healthy tissue and significantly affect patient well-being. In the case of type II autoimmune hypersensitivities, autoreactive antibodies attack the host's own cells or extracellular matrix.
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