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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

CD1d deficiency limits tolerogenic properties of peritoneal macrophages
Fathihah Basri1,# (Graduate student), Sundo Jung 2,# (Professor), Se Hoon Park1 (Graduate student), Se-Ho Park 1,* (Professor)
1Life Sciences, Korea University,
2Biomedical Laboratory Science, Shinhan University
Invariant natural killer T (iNKT) cells are involved in various autoimmune diseases. Although iNKT cells are arthritogenic, transforming growth factor beta (TGFモ)-treated tolerogenic peritoneal macrophages (Tol-pMヵ) 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ヵ can act as tolerogenic antigen presenting cells (APCs) is currently unclear. To determine cellular mechanisms underlying CD1d-dependent tolerogenicity of pMヵ, in vitro and in vivo characteristics of pMヵ were investigated. Unlike dendritic cells or splenic Mヵ, pMヵ 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ヵ from CD1d-deficient mice. In a CIA model of CD1d-deficient mice, adoptively transferred pMヵ from WT mice reduced the severity of arthritis. However, pMヵ from CD1d-deficient mice were unable to reduce the severity of arthritis. Hence, the tolerogenicity of pMヵ is a cell-intrinsic property that is probably conferred by iNKT cells during pMヵ development rather than by interactions of pMヵ with iNKT cells during antigen presentation to cognate T cells.
Abstract, Accepted Manuscript(in press) [Submitted on August 31, 2020, Accepted on December 10, 2020]
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