Related Experiment Video

Updated: Jan 18, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
09:04

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells

Published on: May 22, 2014

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Regulation of ZFP36 by lncOlfr29 promotes inflammation through NLRP3

Wenyue Cheng1, Fan Li1, Yuan Zhang1

  • 1Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China.

Frontiers in Immunology
|September 11, 2025
PubMed
Abstract

Insights

A novel long non-coding RNA, lncOlfr29, promotes inflammation by regulating NLRP3. This discovery offers new therapeutic targets for inflammatory diseases and infections.

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Macrophage function is critical in disease pathogenesis.
  • Identifying novel regulatory factors in macrophages is key for therapeutic development.

Purpose of the Study:

  • To discover and characterize a new regulatory factor in macrophages.
  • To explore the role of this factor in inflammatory diseases.

Main Methods:

  • RNA sequencing identified lncOlfr29.
  • Functional studies involved shRNA, adenovirus, and knockout mice.
  • In vivo models included Salmonella infection and DSS-induced colitis.

Main Results:

  • lncOlfr29 promotes inflammation via NLRP3-mediated IL-1β maturation and pyroptosis.
  • lncOlfr29 enhances resistance to Salmonella infection but increases susceptibility to colitis.
  • lncOlfr29 binds ZFP36, preventing NLRP3 mRNA degradation.

Conclusions:

  • lncOlfr29 regulates NLRP3 expression through ZFP36 interaction.
  • This mechanism provides novel insights for treating inflammatory diseases.
Keywords:
IL-1βNLRP3ZFP36lncOlfr29macrophages

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