Soluble triggering receptor expressed on myeloid cells-1 as a new therapeutic molecule in rheumatoid arthritis

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Abstract

Triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently identified cell surface receptor that is expressed mainly on monocytes and neutrophils, and plays an important role as an amplifier of inflammatory response in acute and chronic inflammatory conditions. Recent studies suggested that TREM-1 contributes to the pathogenesis of rheumatoid arthritis (RA) and therefore TREM-1 could be a new therapeutic target in RA. In addition to its membrane-bound form, a soluble form of TREM-1 (sTREM-1) exists that is liberated by the proteolytic cleavage of membrane-bound form. This soluble form works as decoy receptor to prevent the binding of its ligand to membrane-bound TREM-1 and to inhibit the effect of TREM-1 activation. Proteolytic cleavage of TNF receptor (TNFR) has been reported and soluble TNFR are capable of binding and neutralizing TNF, thus working as natural TNF antagonist. Currently, etanercept, a soluble TNF-receptor fusion protein has been widely used to treat RA. In this report, we suggest that sTREM-1 can be used as a new therapeutic molecule in RA.

Original languageEnglish
Pages (from-to)270-272
Number of pages3
JournalMedical Hypotheses
Volume78
Issue number2
DOIs
Publication statusPublished - 2012 Feb 1

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Myeloid Cells
Rheumatoid Arthritis
Tumor Necrosis Factor Receptors
Membranes
Therapeutics
Cell Surface Receptors
Monocytes
Neutrophils
Ligands
Proteins

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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title = "Soluble triggering receptor expressed on myeloid cells-1 as a new therapeutic molecule in rheumatoid arthritis",
abstract = "Triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently identified cell surface receptor that is expressed mainly on monocytes and neutrophils, and plays an important role as an amplifier of inflammatory response in acute and chronic inflammatory conditions. Recent studies suggested that TREM-1 contributes to the pathogenesis of rheumatoid arthritis (RA) and therefore TREM-1 could be a new therapeutic target in RA. In addition to its membrane-bound form, a soluble form of TREM-1 (sTREM-1) exists that is liberated by the proteolytic cleavage of membrane-bound form. This soluble form works as decoy receptor to prevent the binding of its ligand to membrane-bound TREM-1 and to inhibit the effect of TREM-1 activation. Proteolytic cleavage of TNF receptor (TNFR) has been reported and soluble TNFR are capable of binding and neutralizing TNF, thus working as natural TNF antagonist. Currently, etanercept, a soluble TNF-receptor fusion protein has been widely used to treat RA. In this report, we suggest that sTREM-1 can be used as a new therapeutic molecule in RA.",
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AU - Kim, Tae Hwan

AU - Choi, Sungjae

AU - Lee, Young Ho

AU - Song, Gwan Gyu

AU - Ji, Jong Dae

PY - 2012/2/1

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N2 - Triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently identified cell surface receptor that is expressed mainly on monocytes and neutrophils, and plays an important role as an amplifier of inflammatory response in acute and chronic inflammatory conditions. Recent studies suggested that TREM-1 contributes to the pathogenesis of rheumatoid arthritis (RA) and therefore TREM-1 could be a new therapeutic target in RA. In addition to its membrane-bound form, a soluble form of TREM-1 (sTREM-1) exists that is liberated by the proteolytic cleavage of membrane-bound form. This soluble form works as decoy receptor to prevent the binding of its ligand to membrane-bound TREM-1 and to inhibit the effect of TREM-1 activation. Proteolytic cleavage of TNF receptor (TNFR) has been reported and soluble TNFR are capable of binding and neutralizing TNF, thus working as natural TNF antagonist. Currently, etanercept, a soluble TNF-receptor fusion protein has been widely used to treat RA. In this report, we suggest that sTREM-1 can be used as a new therapeutic molecule in RA.

AB - Triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently identified cell surface receptor that is expressed mainly on monocytes and neutrophils, and plays an important role as an amplifier of inflammatory response in acute and chronic inflammatory conditions. Recent studies suggested that TREM-1 contributes to the pathogenesis of rheumatoid arthritis (RA) and therefore TREM-1 could be a new therapeutic target in RA. In addition to its membrane-bound form, a soluble form of TREM-1 (sTREM-1) exists that is liberated by the proteolytic cleavage of membrane-bound form. This soluble form works as decoy receptor to prevent the binding of its ligand to membrane-bound TREM-1 and to inhibit the effect of TREM-1 activation. Proteolytic cleavage of TNF receptor (TNFR) has been reported and soluble TNFR are capable of binding and neutralizing TNF, thus working as natural TNF antagonist. Currently, etanercept, a soluble TNF-receptor fusion protein has been widely used to treat RA. In this report, we suggest that sTREM-1 can be used as a new therapeutic molecule in RA.

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