CD16+ monocytes control T-cell subset development in immune thrombocytopenia. Academic Article uri icon


MeSH Major

  • Monocytes
  • Purpura, Thrombocytopenic, Idiopathic
  • Receptors, IgG
  • T-Lymphocyte Subsets
  • T-Lymphocytes, Helper-Inducer
  • T-Lymphocytes, Regulatory


  • Immune thrombocytopenia (ITP) results from decreased platelet production and accelerated platelet destruction. Impaired CD4(+) regulatory T-cell (Treg) compartment and skewed Th1 and possibly Th17 responses have been described in ITP patients. The trigger for aberrant T-cell polarization remains unknown. Because monocytes have a critical role in development and polarization of T-cell subsets, we explored the contribution of monocyte subsets in control of Treg and Th development in patients with ITP. Unlike circulating classic CD14(hi)CD16(-) subpopulation, the CD16(+) monocyte subset was expanded in ITP patients with low platelet counts on thrombopoietic agents and positively correlated with T-cell CD4(+)IFN-γ(+) levels, but negatively with circulating CD4(+)CD25(hi)Foxp3(+) and IL-17(+) Th cells. Using a coculture model, we found that CD16(+) ITP monocytes promoted the expansion of IFN-γ(+)CD4(+) cells and concomitantly inhibited the proliferation of Tregs and IL-17(+) Th cells. Th-1-polarizing cytokine IL-12, secreted after direct contact of patient T-cell and CD16(+) monocytes, was responsible for the inhibitory effect on Treg and IL-17(+)CD4(+) cell proliferation. Our findings are consistent with ITP CD16(+) monocytes promoting Th1 development, which in turn negatively regulates IL-17 and Treg induction. This underscores the critical role of CD16(+) monocytes in the generation of potentially pathogenic Th responses in ITP.

publication date

  • October 18, 2012



  • Academic Article



  • eng

PubMed Central ID

  • PMC3476543

PubMed ID

  • 22915651

Additional Document Info

start page

  • 3326

end page

  • 35


  • 120


  • 16