CD122 blockade restores immunological tolerance in autoimmune type 1 diabetes via multiple mechanisms

JCI Insight. 2018 Jan 25;3(2):e96600. doi: 10.1172/jci.insight.96600.

Abstract

Signaling through IL-2/IL-15Rβ (CD122) is essential for the differentiation and function of T cells and NK cells. A mAb against CD122 has been implicated to suppress autoimmune type 1 diabetes (T1D) development in animal models. However, the mechanisms remain poorly understood. We find that in vivo administration of an anti-CD122 mAb (CD122 blockade) restores immune tolerance in nonobese diabetic (NOD) mice via multiple mechanisms. First, CD122 blockade selectively ablates pathogenic NK cells and memory phenotype CD8+ T cells from pancreatic islets. In contrast, islet CD4+Foxp3+ Tregs are only mildly affected. Second, CD122 blockade suppresses IFN-γ production in islet immune cells. Third, CD122 blockade inhibits the conversion of islet Th17 cells into diabetogenic Th1 cells. Furthermore, a combination of anti-CD122 mAb and Treg-trophic cytokines (IL-2 or IL-33) enhances the abundance and function of islet Tregs. In summary, these data provide crucial mechanistic insights into CD122 blockade-mediated immunoregulation and support therapeutic benefits of this combinational treatment in T1D.

Keywords: Autoimmunity; Cytokines; Diabetes; Inflammation; NK cells.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / administration & dosage*
  • Antibodies, Monoclonal / immunology
  • Antibodies, Monoclonal / isolation & purification
  • CD8-Positive T-Lymphocytes / drug effects
  • CD8-Positive T-Lymphocytes / immunology
  • Diabetes Mellitus, Type 1 / drug therapy*
  • Diabetes Mellitus, Type 1 / immunology
  • Disease Models, Animal
  • Drug Therapy, Combination / methods
  • Female
  • Hybridomas
  • Immune Tolerance / drug effects*
  • Immunologic Factors / administration & dosage*
  • Interleukin-2 / administration & dosage
  • Interleukin-2 Receptor beta Subunit / antagonists & inhibitors*
  • Interleukin-2 Receptor beta Subunit / immunology
  • Interleukin-33 / administration & dosage
  • Islets of Langerhans / cytology
  • Islets of Langerhans / immunology
  • Killer Cells, Natural / drug effects
  • Killer Cells, Natural / immunology
  • Mice
  • Mice, Inbred NOD
  • Rats
  • Rats, Sprague-Dawley
  • Recombinant Proteins / administration & dosage
  • T-Lymphocytes, Regulatory / drug effects
  • T-Lymphocytes, Regulatory / immunology
  • Th1 Cells / drug effects
  • Th1 Cells / immunology
  • Th17 Cells / drug effects
  • Th17 Cells / immunology
  • Treatment Outcome

Substances

  • Antibodies, Monoclonal
  • IL2 protein, human
  • IL33 protein, human
  • Il2rb protein, mouse
  • Immunologic Factors
  • Interleukin-2
  • Interleukin-2 Receptor beta Subunit
  • Interleukin-33
  • Recombinant Proteins