Abstract
AbstractImmune thrombocytopenia (ITP) is an autoimmune bleeding disorder characterized by low platelet counts. First-line treatment includes intravenous immunoglobulin (IVIg), however, its working mechanism remains incompletely understood. We investigated splenic and thymic dendritic cell (DC) subsets upon IVIg treatment in a well-characterized active murine model of ITP. During active disease, there was a significant peripheral deficiency of splenic tolerizing SIRPα+ DCs which could be rescued by IVIg therapy, increasing platelet counts. These splenic tolerizing DC changes were associated with an abrogation of the thymic-retention of tolerizing DCs, suggesting that IVIg may raise platelet counts in ITP by modulating peripheral numbers of tolerizing DCs.
Original language | English |
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Pages (from-to) | 521-524 |
Journal | Platelets |
Volume | 28 |
Issue number | 5 |
DOIs | |
Publication status | Published - 2017 Jul 4 |
Externally published | Yes |