KMID : 0624620210540040209
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BMB Reports 2021 Volume.54 No. 4 p.209 ~ p.214
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CD1d deficiency limits tolerogenic properties of peritoneal macrophages
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Basri Fathihah
Jung Sun-Do Park Se-Hoon Park Se-Hoon
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Abstract
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Invariant natural killer T (iNKT) cells are involved in various autoimmune diseases. Although iNKT cells are arthritogenic, transforming growth factor beta (TGF¥â)-treated tolerogenic peritoneal macrophages (Tol-pM¥õ) 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 pM¥õ can act as tolerogenic antigen presenting cells (APCs) is currently unclear. To determine cellular mechanisms underlying CD1d-dependent tolerogenicity of pM¥õ, in vitro and in vivo characteristics of pM¥õ were investigated. Unlike dendritic cells or splenic M¥õ, pM¥õ from CD1d+/- mice showed lower expression levels of costimulatory molecule CD86 and produced lower amounts of inflammatory cytokines upon lipopolysaccharide (LPS) stimulation compared to pM¥õ from CD1d-deficient mice. In a CIA model of CD1d-deficient mice, adoptively transferred pM¥õ from WT mice reduced the severity of arthritis. However, pM¥õ from CD1d-deficient mice were unable to reduce the severity of arthritis. Hence, the tolerogenicity of pM¥õ is a cell-intrinsic property that is probably conferred by iNKT cells during pM¥õ development rather than by interactions of pM¥õ with iNKT cells during antigen presentation to cognate T cells.
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KEYWORD
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CD1d, CIA, NKT cells, Peritoneal macrophage, Rheumatoid arthritis
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