Thymic-derived tolerizing dendritic cells are upregulated in the spleen upon treatment with intravenous immunoglobulin in a murine model of immune thrombocytopenia.

Authors:
John W Semple
John W Semple
Lund University
Professor of Transfusion Medicine
Lund, Skane | Sweden

Platelets 2017 Jul 25;28(5):521-524. Epub 2016 Nov 25.

a The Toronto Platelet Immunobiology Group , Keenan Research Centre for Biomedical Science of St. Michael's Hospital , Toronto , ON , Canada.

Immune 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.

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http://dx.doi.org/10.1080/09537104.2016.1246718DOI Listing
July 2017
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References

(Supplied by CrossRef)

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Front Immunol 2014

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