CD1d deficiency limits tolerogenic properties of peritoneal macrophages

Fathihah Basri, Sundo Jung, Se Hoon Park, Se Ho Park

Research output: Contribution to journalArticlepeer-review

Abstract

Invariant natural killer T (iNKT) cells are involved in various autoimmune diseases. Although iNKT cells are arthritogenic, transforming growth factor beta (TGFβ)-treated tolerogenic peritoneal macrophages (Tol-pMφ) from wild-type (WT) mice are more tolerogenic than those from CD1d knock-out iNKT cell-deficient mice in a collagen-induced arthritis (CIA) model. The underlying mechanism by which pMφ can act as tolerogenic antigen presenting cells (APCs) is currently unclear. To determine cellular mechanisms underlying CD1d-dependent tolerogenicity of pMφ, in vitro and in vivo characteristics of pMφ were investigated. Unlike dendritic cells or splenic Mφ, pMφ from CD1d+/− mice showed lower expression levels of costimulatory molecule CD86 and produced lower amounts of inflammatory cytokines upon lipopolysaccharide (LPS) stimulation compared to pMφ from CD1d-deficient mice. In a CIA model of CD1d-deficient mice, adoptively transferred pMφ from WT mice reduced the severity of arthritis. However, pMφ from CD1d-deficient mice were unable to reduce the severity of arthritis. Hence, the tolerogenicity of pMφ is a cell-intrinsic property that is probably conferred by iNKT cells during pMφ development rather than by interactions of pMφ with iNKT cells during antigen presentation to cognate T cells. [BMB Reports 2021; 54(4): 209-214]

Original languageEnglish
Pages (from-to)209-214
Number of pages6
JournalBMB reports
Volume54
Issue number4
DOIs
Publication statusPublished - 2021

Keywords

  • CD1d
  • CIA
  • NKT cells
  • Peritoneal macrophage
  • Rheumatoid arthritis

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

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