CD1d deficiency limits tolerogenic properties of peritoneal macrophages
- Authors
- Basri, Fathihah; Jung, Sundo; Park, Se Hoon; Park, Se-Ho
- Issue Date
- 30-4월-2021
- Publisher
- KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
- Keywords
- CD1d; CIA; NKT cells; Peritoneal macrophage; Rheumatoid arthritis
- Citation
- BMB REPORTS, v.54, no.4, pp.209 - 214
- Indexed
- SCIE
SCOPUS
KCI
OTHER
- Journal Title
- BMB REPORTS
- Volume
- 54
- Number
- 4
- Start Page
- 209
- End Page
- 214
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/128197
- DOI
- 10.5483/BMBRep.2021.54.4.183
- ISSN
- 1976-6696
- Abstract
- Invariant natural killer T (iNKT) cells are involved in various autoimmune diseases. Although iNKT cells are arthritogenic, transforming growth factor beta (TGF beta)-treated tolerogenic peritoneal macrophages (Tol-pM Phi) 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 Phi can act as tolerogenic antigen presenting cells (APCs) is currently unclear. To determine cellular mechanisms underlying CD1d-dependent tolerogenicity of pM Phi, in vitro and in vivo characteristics of pM Phi were investigated. Unlike dendritic cells or splenic M Phi, pM Phi 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 Phi from CD1d-deficient mice. In a CIA model of CD1d-deficient mice, adoptively transferred pM Phi from WT mice reduced the severity of arthritis. However, pM Phi from CD1d-deficient mice were unable to reduce the severity of arthritis. Hence, the tolerogenicity of pM Phi is a cell-intrinsic property that is probably conferred by iNKT cells during pM Phi development rather than by interactions of pM Phi with iNKT cells during antigen presentation to cognate T cells.
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Collections - College of Life Sciences and Biotechnology > Division of Life Sciences > 1. Journal Articles
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