Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis

Yong du; Tianfu Wu; Xin J. Zhou; Laurie S. Davis; Chandra Mohan

doi:10.1007/s10753-016-0351-1

Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis

Yong du, Tianfu Wu, Xin J. Zhou, Laurie S. Davis, Chandra Mohan

Research output: Contribution to journal › Article › peer-review

9 Scopus citations

Abstract

CD354, Triggering Receptor of Myeloid Cells-1 (TREM-1), is a potent amplifier of myeloid immune responses. Our goal was to determine the expression and function of TREM-1 in immune-mediated nephritis. An anti-glomerular basement membrane antibody (anti-GBM)-induced nephritis model was employed, where mice were sensitized with rabbit IgG followed by anti-GBM serum to induce disease. Anti-GBM-treated 129x1/svJ mice developed severe nephritis whereas C57BL/6 (B6) mice were resistant to disease. Anti-GBM disease resulted in elevated renal TREM-1 messenger RNA (mRNA) and protein levels and increased urine TREM-1 levels in 129x1/svJ. TREM-1 blockade with an inhibitory peptide, LP17, inhibited proteinuria and renal disease as measured by glomerulonephritis class, severity of tubulointerstitial disease, crescent formation, and inflammatory cell infiltrates. In sum, TREM-1 is upregulated in renal inflammation and plays a vital role in driving disease. Thus, TREM-1 blockade emerges as a potential therapeutic avenue for immune-mediated renal diseases such as lupus nephritis.

Original language	English (US)
Pages (from-to)	1169-1176
Number of pages	8
Journal	Inflammation
Volume	39
Issue number	3
DOIs	https://doi.org/10.1007/s10753-016-0351-1
State	Published - Jun 1 2016

Keywords

SLE, systemic lupus erythematosus
Triggering Receptor Expressed by Myeloid Cells-1 (TREM-1)
anti-glomerular basement membrane antibody-induced nephritis
immune-mediated nephritis
immunotherapy

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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10.1007/s10753-016-0351-1

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title = "Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis",

abstract = "CD354, Triggering Receptor of Myeloid Cells-1 (TREM-1), is a potent amplifier of myeloid immune responses. Our goal was to determine the expression and function of TREM-1 in immune-mediated nephritis. An anti-glomerular basement membrane antibody (anti-GBM)-induced nephritis model was employed, where mice were sensitized with rabbit IgG followed by anti-GBM serum to induce disease. Anti-GBM-treated 129x1/svJ mice developed severe nephritis whereas C57BL/6 (B6) mice were resistant to disease. Anti-GBM disease resulted in elevated renal TREM-1 messenger RNA (mRNA) and protein levels and increased urine TREM-1 levels in 129x1/svJ. TREM-1 blockade with an inhibitory peptide, LP17, inhibited proteinuria and renal disease as measured by glomerulonephritis class, severity of tubulointerstitial disease, crescent formation, and inflammatory cell infiltrates. In sum, TREM-1 is upregulated in renal inflammation and plays a vital role in driving disease. Thus, TREM-1 blockade emerges as a potential therapeutic avenue for immune-mediated renal diseases such as lupus nephritis.",

keywords = "SLE, systemic lupus erythematosus, Triggering Receptor Expressed by Myeloid Cells-1 (TREM-1), anti-glomerular basement membrane antibody-induced nephritis, immune-mediated nephritis, immunotherapy",

author = "Yong du and Tianfu Wu and Zhou, {Xin J.} and Davis, {Laurie S.} and Chandra Mohan",

note = "Publisher Copyright: {\textcopyright} 2016, The Author(s).",

year = "2016",

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doi = "10.1007/s10753-016-0351-1",

language = "English (US)",

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AU - du, Yong

AU - Wu, Tianfu

AU - Zhou, Xin J.

AU - Davis, Laurie S.

AU - Mohan, Chandra

PY - 2016/6/1

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N2 - CD354, Triggering Receptor of Myeloid Cells-1 (TREM-1), is a potent amplifier of myeloid immune responses. Our goal was to determine the expression and function of TREM-1 in immune-mediated nephritis. An anti-glomerular basement membrane antibody (anti-GBM)-induced nephritis model was employed, where mice were sensitized with rabbit IgG followed by anti-GBM serum to induce disease. Anti-GBM-treated 129x1/svJ mice developed severe nephritis whereas C57BL/6 (B6) mice were resistant to disease. Anti-GBM disease resulted in elevated renal TREM-1 messenger RNA (mRNA) and protein levels and increased urine TREM-1 levels in 129x1/svJ. TREM-1 blockade with an inhibitory peptide, LP17, inhibited proteinuria and renal disease as measured by glomerulonephritis class, severity of tubulointerstitial disease, crescent formation, and inflammatory cell infiltrates. In sum, TREM-1 is upregulated in renal inflammation and plays a vital role in driving disease. Thus, TREM-1 blockade emerges as a potential therapeutic avenue for immune-mediated renal diseases such as lupus nephritis.

AB - CD354, Triggering Receptor of Myeloid Cells-1 (TREM-1), is a potent amplifier of myeloid immune responses. Our goal was to determine the expression and function of TREM-1 in immune-mediated nephritis. An anti-glomerular basement membrane antibody (anti-GBM)-induced nephritis model was employed, where mice were sensitized with rabbit IgG followed by anti-GBM serum to induce disease. Anti-GBM-treated 129x1/svJ mice developed severe nephritis whereas C57BL/6 (B6) mice were resistant to disease. Anti-GBM disease resulted in elevated renal TREM-1 messenger RNA (mRNA) and protein levels and increased urine TREM-1 levels in 129x1/svJ. TREM-1 blockade with an inhibitory peptide, LP17, inhibited proteinuria and renal disease as measured by glomerulonephritis class, severity of tubulointerstitial disease, crescent formation, and inflammatory cell infiltrates. In sum, TREM-1 is upregulated in renal inflammation and plays a vital role in driving disease. Thus, TREM-1 blockade emerges as a potential therapeutic avenue for immune-mediated renal diseases such as lupus nephritis.

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Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis

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