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 journalArticle

2 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 languageEnglish (US)
Pages (from-to)1-8
Number of pages8
JournalInflammation
DOIs
Publication statusAccepted/In press - Apr 15 2016

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ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

du, Y., Wu, T., Zhou, X. J., Davis, L. S., & Mohan, C. (Accepted/In press). Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis. Inflammation, 1-8. https://doi.org/10.1007/s10753-016-0351-1