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Itaconate modulates immune responses via inhibition of peroxiredoxin 5

ABSTRACT: Wild type and Irg1 knockout mouse bone marrow derived macrophages (BMDMs) were processed with a redox proteomics workflow and analyzed by LC-MS/MS with TMT based quantification.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Wei-Jun Qian

PROVIDER: MSV000093232 | MassIVE | Wed Nov 01 16:52:00 GMT 2023

SECONDARY ACCESSION(S): PXD046597

REPOSITORIES: MassIVE

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Itaconate modulates immune responses via inhibition of peroxiredoxin 5.

Paulenda Tomas T Echalar Barbora B Potuckova Lucie L Vachova Veronika V Kleverov Denis A DA Mehringer Johannes J Potekhina Ekaterina E Jacoby Alex A Sen Devashish D Nelson Chris C Stegeman Rick R Sukhov Vladimir V Kemper Danielle D Lichti Cheryl F CF Day Nicholas J NJ Zhang Tong T Husarcikova Kamila K Bambouskova Monika M Fremont Daved H DH Qian Wei-Jun WJ Djuranovic Sergej S Pavlovic-Djuranovic Slavica S Belousov Vsevolod V VV Krezel Andrzej M AM Artyomov Maxim N MN

Nature metabolism 20250418 6

The immunoregulatory metabolite itaconate accumulates in innate immune cells upon Toll-like receptor stimulation. In response to macrophage activation by lipopolysaccharide, itaconate inhibits inflammasome activation and boosts type I interferon signalling; however, the molecular mechanism of this immunoregulation remains unclear. Here, we show that the enhancement of type I interferon secretion by itaconate depends on the inhibition of peroxiredoxin 5 and on mitochondrial reactive oxygen specie ...[more]

PMID: 40251412

Similar Datasets

Itaconate modulates immune responses via inhibition of peroxiredoxins

Project description:Itaconate is a natural mild electrophile, able to modify free thiols in proteins upon activation. We submit two datasets investigating peptides modified by itaconate. Experiment001 contains data obtained from endogenous itaconate producing WT or itaconate incompetent Irg1-/- Bone marrow-derived macrophages stimulated with LPS for 24h. The second dataset from Experiment002 contains data obtained from WT Bone marrow-derived macrophages treated with media or 5 mM itaconic acid for 16h.

2023-11-28 | MSV000093522 | MassIVE

Itaconate modulates immune responses via inhibition of peroxiredoxin 5

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Itaconate modulates immune responses via inhibition of peroxiredoxin 5

Project description:Itaconate modulates immune responses via inhibition of peroxiredoxin 5

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IRG1/itaconate axis modulates lung tumor microenvironment via pentose phosphate pathway [sav24]

Project description:Tumor-associated macrophages (TAMs) are an important component of the immune milieu within the lung tumor microenvironment (TME) and have both tumor-promoting and tumor-inhibiting functions. However, the exact mechanisms underlying TAM-mediated inhibition of tumor development are still unknown. Itaconate is one of the main metabolites produced by the enzyme immune responsive gene 1 (IRG1) during a pro-inflammatory response. Single cell RNA-seq studies show that macrophages are the major immune cells for Irg1 expression in human and mouse lung tumors. Both Irg1-deficient mice and transplantation of Irg1-depleted bone marrow resulted in increased development of lung tumors in Kras and orthotopic mouse models, suggesting the anti-tumor function of Irg1-associated macrophages. On the other hand, 4-octyl-itaconate (octyl-Ita) reduces lung tumor development in lung cancer cell lines in vitro, in vivo models of lung cancer, and ex vivo using human tumor precision-cut lung slices. Mechanistically, IRG1/itaconate induces a metabolic shift in cancer cells and pro-tumor macrophages, specifically through inhibition of the pentose phosphate pathway (PPP). An integrative analysis of metabolomics, transcriptomics and proteomics identified glucose-6-phosphate dehydrogenase (G6PD) as the primary target for the antiproliferative effect of IRG1/itaconate. IRG1/Itaconate inhibited G6PD activity without affecting G6PD expression in Irg1-deficient mice and octyl Ita-treated lung cancer models. The novel inhibitory effects of IRG1/Itaconate and Octyl Ita on G6PD activity and PPP metabolism can not only suppress cancer cell proliferation in a non-cell-autonomous manner, but also re-educate pro-tumor macrophages into anti-tumor macrophages in a cell-autonomous manner. Our results suggest that octyl Ita is an effective anti-tumor metabolite with potential therapeutic application in lung cancer.

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IRG1/itaconate axis modulates lung tumor microenvironment via pentose phosphate pathway [sav25]

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Nur77-deficiency in bone marrow-derived macrophages modulates inflammatory responses, extracellular matrix homeostasis, phagocytosis and tolerance

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Piezo1 mediated mechanotransduction modulates macrophages proliferation during bone remodeling via PI3K-AKT-Ccnd1 axis

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