Myeloid-Derived Suppressor Cells Induce the Expansion of Regulatory B Cells and Ameliorate Autoimmunity in the Sanroque Mouse Model of Systemic Lupus Erythematosus

Arthritis Rheumatol. 2016 Nov;68(11):2717-2727. doi: 10.1002/art.39767.

Abstract

Objective: This study was undertaken to assess the effect of myeloid-derived suppressor cells (MDSCs) on various B cell subsets, including regulatory B cells, as well as to assess the potential therapeutic effects of MDSC infusion in an animal model of systemic lupus erythematosus (SLE).

Methods: Splenocytes were cultured with MDSCs, and the populations of various B cells and effector T cell subsets were analyzed by flow cytometry. Lupus mice (roquinsan/san mice) were treated intravenously with MDSCs obtained from C57BL/6 mice, and the levels of serum autoantibodies, degree of proteinuria, histologic changes in the kidney, and populations of various B cell and T cell subsets in the spleen were analyzed.

Results: Coculture of MDSCs with splenocytes from C57BL/6 mice resulted in an expansion of the population of interleukin-10-producing B cells. The expansion of regulatory B cells was completely blocked by the addition of NG -monomethyl-l-arginine, an inhibitor of inducible nitric oxide synthase (iNOS). Infusion of MDSCs resulted in a reduction of serum anti-double-stranded DNA antibody levels and degree of proteinuria and an improvement in renal pathology in the roquinsan/san mice. MDSC coculture also resulted in a decrease in the population of effector B cells, such as germinal center B cells and plasma cells. Moreover, infusion of MDSCs resulted in an expansion of the regulatory B cell population as well as a decrease in follicular helper T cells, Th1 cells, and Th17 cells in the spleens of roquinsan/san mice.

Conclusion: Our results indicate the MDSCs induce expansion of regulatory B cells via iNOS and ameliorate autoimmunity in a murine model of SLE. These findings indicate that MDSCs may be a promising therapeutic strategy for targeting B cell-mediated autoimmune diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Antinuclear / immunology*
  • Autoantibodies / immunology
  • Autoimmunity / drug effects
  • Autoimmunity / immunology*
  • B-Lymphocyte Subsets / immunology*
  • B-Lymphocytes, Regulatory / drug effects
  • B-Lymphocytes, Regulatory / immunology*
  • Coculture Techniques
  • DNA / immunology
  • Disease Models, Animal
  • Enzyme Inhibitors / pharmacology
  • Germinal Center
  • Interleukin-10 / immunology
  • Kidney / immunology
  • Kidney / pathology
  • Lupus Erythematosus, Systemic / immunology*
  • Lupus Nephritis / immunology
  • Mice
  • Mice, Inbred C57BL
  • Myeloid-Derived Suppressor Cells / immunology*
  • NG-Nitroarginine Methyl Ester / pharmacology
  • Nitric Oxide Synthase Type II / antagonists & inhibitors
  • Plasma Cells / immunology
  • Proteinuria / immunology
  • Spleen / cytology
  • Spleen / immunology
  • T-Lymphocytes / immunology*
  • T-Lymphocytes, Helper-Inducer / immunology
  • Th1 Cells / immunology
  • Th17 Cells / immunology
  • Ubiquitin-Protein Ligases / genetics

Substances

  • Antibodies, Antinuclear
  • Autoantibodies
  • Enzyme Inhibitors
  • IL10 protein, mouse
  • Interleukin-10
  • DNA
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • Rc3h1 protein, mouse
  • Ubiquitin-Protein Ligases
  • NG-Nitroarginine Methyl Ester