IL-2/anti-IL-2 complexes ameliorate lupus nephritis by expansion of CD4+CD25+Foxp3+ regulatory T cells

Kidney Int. 2017 Mar;91(3):603-615. doi: 10.1016/j.kint.2016.09.022. Epub 2016 Dec 1.

Abstract

Adoptive transfer of regulatory T cells (Tregs) can delay disease progression and reduce mortality in lupus-prone mice. Here, we tested whether complex (IL-2C) consisting of IL-2 and anti-IL-2 monoclonal antibody (JES6-1) ameliorates lupus nephritis by expanding Tregs as an alternative to problematic Treg infusion therapy. IL-2C treatment of NZB/W F1 mice induced an effective and sustained expansion of CD4+CD25+Foxp3+ Tregs in both the kidneys and spleen along with decreased renal infiltration of T cells, B cells, and innate immune cells. Compared with controls, mice treated with IL-2C showed reduced proteinuria and fewer acute and chronic renal pathological lesions with improved renal function and survival. IL-2C significantly attenuated glomerular and tubular injury, vasculitis scores, and renal deposition of IgG and C3. Disease activity markers, such as high levels of anti-dsDNA antibodies and immunoglobulin levels, and low levels of complement were improved in sera of IL-2C-treated mice. IL-2C treatment decreased renal expression of TNF-α and IL-6, and the frequencies of IFN-γ+CD4+ and IL-17A+CD4+ T cells in both the kidneys and spleen. Depletion of Tregs by anti-CD25 antibodies abrogated the beneficial effects of IL-2C. When compared with combination therapy of steroid and mycophenolate mofetil, IL-2C treatment showed similar or better outcomes. Thus, IL-2C protected lupus-prone mice against lupus nephritis by expanding Tregs. Hence, IL-2C could have therapeutic potential in lupus nephritis.

Keywords: interleukin-2/anti-interleukin-2 complex; lupus nephritis; regulatory T cells.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / pharmacology*
  • Cell Proliferation / drug effects*
  • Cytokines / immunology
  • Cytokines / metabolism
  • Disease Models, Animal
  • Drug Therapy, Combination
  • Forkhead Transcription Factors / immunology
  • Forkhead Transcription Factors / metabolism*
  • Immunosuppressive Agents / pharmacology*
  • Inflammation Mediators / immunology
  • Inflammation Mediators / metabolism
  • Interleukin-2 / antagonists & inhibitors
  • Interleukin-2 / immunology
  • Interleukin-2 / pharmacology*
  • Interleukin-2 Receptor alpha Subunit / antagonists & inhibitors
  • Interleukin-2 Receptor alpha Subunit / immunology
  • Interleukin-2 Receptor alpha Subunit / metabolism*
  • Kidney / drug effects*
  • Kidney / immunology
  • Kidney / metabolism
  • Kidney / physiopathology
  • Lupus Nephritis / immunology
  • Lupus Nephritis / metabolism
  • Lupus Nephritis / physiopathology
  • Lupus Nephritis / prevention & control*
  • Mice
  • Proteinuria / immunology
  • Proteinuria / metabolism
  • Proteinuria / physiopathology
  • Proteinuria / prevention & control
  • Recovery of Function
  • Signal Transduction / drug effects
  • Spleen / drug effects
  • Spleen / immunology
  • Spleen / metabolism
  • T-Lymphocytes, Regulatory / drug effects*
  • T-Lymphocytes, Regulatory / immunology
  • T-Lymphocytes, Regulatory / metabolism
  • Time Factors

Substances

  • Antibodies, Monoclonal
  • Cytokines
  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • Immunosuppressive Agents
  • Inflammation Mediators
  • Interleukin-2
  • Interleukin-2 Receptor alpha Subunit