AI Article Synopsis
- The article examines the complex immune mechanisms involved in immune thrombocytopenia (ITP) and questions whether immune abnormalities are a cause or a consequence of the disease.
- It highlights the roles of three key immune cells—antigen-presenting cells (APC), T cells, and B cells—in the development and persistence of ITP, especially in its chronic form.
- Additionally, the review explores recent genetic findings related to ITP and evaluates relevant animal models used in research.
Article Abstract
Over the past decades, a wealth of information has been reported about the pathogenic features of immune thrombocytopenia (ITP). To this day, however, it is unclear whether the immune abnormalities associated with ITP play causative roles in the disease or are secondary epiphenomena brought on by the inflammatory processes that are associated with the disorder. Like the majority of all autoimmune diseases, ITP is an organ-specific disease and abnormalities in immune cell types, such as antigen-presenting cells (APC), T cells and B cells have been shown to play some sort of role in the initiation and/or perpetuation of the disease. This review will discuss recent advances in understanding three immune cells important in ITP pathophysiology: APC, T cells and B cells, and will review how they interact with each other to initiate and perpetuate ITP, particularly the chronic form of the disorder. It will also focus on new data related to the genetics of the disorder and discuss relevant animal models of ITP.
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| http://dx.doi.org/10.1111/bjh.12480 | DOI Listing |
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