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Immune thrombocytopenia: what can the systems biology and systems physiology offer?

Immune thrombocytopenia (ITP) is an acquired bleeding disorder of autoimmune pathophysiology. The causes of ITP could be related to other pathology (viral, bacterial, or systemic), or ITP could develop without any apparent reason. While the immune system dysregulation mechanisms in ITP were described, its etiology remains unclear. Moreover, all existing treatment approaches are not specific for ITP, and its action is highly patient- specific. Here we describe recent findings in the origins and development of ITP and discuss novel experimental and theoretical approaches to diagnosing ITP and predicting therapy effects.

Schematic of immune thrombocytopenia mechanisms. The thrombocytopenia in patients could be caused by both T-cells cytotoxicity (CTLs are more active because T-regulatory cells and T-helpers provide dysregulated stimuli) and B-cells antibody production (plasma cells are producing antiplatelet antibodies of IgG and IgM classes; B-regulatory cells provide more activating signals to B-cells to produce antibodies). CTLs specifically attack platelets and induce their apoptosis. Antibodies from plasma cells opsonize platelets. Consecutively, opsonized platelets are eliminated through the spleen. CTLs – cytotoxic T-lymphocytes; Treg – T-regulatory cell; Th – T-helper; Breg – B-regulatory cell; BAFF – B-cell activating factor.
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#autoimmunity#ITP#platelets#acute/chronic ITP#computational modeling#murine models

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