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

Authors
  • Kapur, Rick1, 2
  • Aslam, Rukhsana1
  • Kim, Michael1
  • Guo, Li1
  • Ni, Heyu1, 2, 3, 4
  • Segel, George B5
  • Semple, John W1, 2, 3, 4, 6
  • 1 a The Toronto Platelet Immunobiology Group , Keenan Research Centre for Biomedical Science of St. Michael's Hospital , Toronto , ON , Canada. , (Canada)
  • 2 b Canadian Blood Services , Toronto , ON , Canada. , (Canada)
  • 3 c Department of Medicine , University of Toronto , Toronto , ON , Canada. , (Canada)
  • 4 d Department of Laboratory Medicine and Pathobiology , University of Toronto , Toronto , ON , Canada. , (Canada)
  • 5 e Department of Medicine , University of Rochester School of Medicine , Rochester , NY , USA.
  • 6 f Department of Pharmacology , University of Toronto , Toronto , ON , Canada. , (Canada)
Type
Published Article
Journal
Platelets
Publisher
Informa UK (Taylor & Francis)
Publication Date
Jul 01, 2017
Volume
28
Issue
5
Pages
521–524
Identifiers
DOI: 10.1080/09537104.2016.1246718
PMID: 27885866
Source
Medline
Keywords
License
Unknown

Abstract

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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