Platelets convert peripheral blood circulating monocytes to regulatory cells via immunoglobulin G and activating-type Fcγ receptors

BMC Immunol. 2015 Apr 21;16:20. doi: 10.1186/s12865-015-0086-z.


Background: Monocytes and macrophages produce interleukin (IL)-10, an immunoregulatory cytokine and a potent therapeutic tool for immune disorders. Augmentation of IL-10 production with a concomitant reduction of proinflammatory cytokines in macrophages in vitro is attained by doubly stimulating the cells with a toll-like receptor ligand and immunoglobulin (Ig)G immune complexes, a response known as that of regulatory (or alternatively activated/M2) macrophages. However, it has not been explored sufficiently how such a regulatory response could be exploited for anti-inflammation. Our objective is to find a potential way or condition for augmenting IL-10 by monocytes/macrophages in vivo and in vitro.

Results: We show that platelets, when they are opsonized with IgG, can convert human peripheral blood circulating monocytes to IL-10-producing regulatory monocytes in vitro and also in a murine in vivo model. Co-culturing of platelets and monocytes in the presence of anti-integrin IgG and a bacterial lipopolysaccharide augmented IL-10 production via a direct interaction between platelets and monocytes. This novel way of enhancing IL-10 was mediated by activating-type Fc receptors for IgG.

Conclusion: These findings indicate that the IgG-bound platelet-induced conversion of monocytes to regulatory cells might provide a novel strategy for controlling inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibodies, Blocking / pharmacology
  • Blood Circulation
  • Blood Platelets / drug effects
  • Blood Platelets / immunology*
  • Cell Communication / drug effects
  • Cell Differentiation / drug effects
  • Cells, Cultured
  • Coculture Techniques
  • Humans
  • Immunoglobulin G / metabolism*
  • Immunomodulation
  • Integrins / immunology
  • Integrins / metabolism
  • Interleukin-10 / metabolism*
  • Lipopolysaccharides / metabolism
  • Monocytes / drug effects
  • Monocytes / immunology*
  • Receptors, IgG / metabolism*


  • Antibodies, Blocking
  • Immunoglobulin G
  • Integrins
  • Lipopolysaccharides
  • Receptors, IgG
  • Interleukin-10