Defective regulatory B-cell compartment in patients with immune thrombocytopenia Academic Article uri icon

Overview

MeSH Major

  • Antigen Presentation
  • B-Lymphocytes, Regulatory
  • Monocytes
  • Purpura, Thrombocytopenic, Idiopathic

abstract

  • B lymphocytes producing antiplatelet autoantibodies play a major role in autoimmune thrombocytopenia (ITP). However, certain B cells, including the human CD19(+)CD24(hi)CD38(hi) subpopulation, possess regulatory functions mediated partly by IL-10. In a cohort of chronic ITP patients with low platelet counts who consisted of patients off treatment, we found a lower frequency of CD19(+)CD24(hi)CD38(hi) in the peripheral compartment of nonsplenectomized patients (P = .03). IL-10 expression after activation was decreased in all ITP circulating CD19(+) subpopulations (P < .03), and inhibition of monocyte TNF-α expression by activated B cells was reduced in patients with platelet numbers of < 50 × 10(9) cells/L (P = .001), indicating that regulatory B cells of patients with ITP are functionally impaired in their ability to dampen monocyte activation. Interestingly, in nonsplenectomized patients whose platelet counts were elevated after treatment with thrombopoietic agents, the frequency of CD19(+)CD24(hi)CD38(hi) B cells was increased compared with those before treatment (P = .02). Altogether, these data indicate a compromised regulatory B-cell compartment as an additional defect in immune regulation in patients with chronic ITP that may be restored in responders to thrombopoietic treatment.

publication date

  • October 18, 2012

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC3476542

Digital Object Identifier (DOI)

  • 10.1182/blood-2012-05-432575

PubMed ID

  • 22859611

Additional Document Info

start page

  • 3318

end page

  • 25

volume

  • 120

number

  • 16