ArticleBlood advances2021
BCL-XL antagonism selectively reduces neutrophil life span within inflamed tissues without causing neutropenia.
Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Environmental benzene exposure induces a conserved neutrophil degranulation program across species.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Co-targeting of epigenetic regulators and BCL-XL improves efficacy of immune checkpoint blockade therapy in multiple solid tumors.Molecular cancer · 2025Article
- New insights into constitutive neutrophil death.Cell death discovery · 2025Review
- Article
- Drug delivery for age-related bone diseases: From therapeutic targets to common and emerging therapeutic strategies.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Review
- Protein isoform-centric therapeutics: expanding targets and increasing specificity.Nature reviews. Drug discovery · 2024Review
- Bcl-xL targeting eliminates ageing tumor-promoting neutrophils and inhibits lung tumor growth.EMBO molecular medicine · 2024Article
- Leucocyte Abnormalities in Synovial Fluid of Degenerative and Inflammatory Arthropathies.International journal of molecular sciences · 2023Article
- Autoimmune Neutropenias: Update on Clinical and Biological Features in Children and Adults.HemaSphere · 2023Review
- Programmed cell death: the pathways to severe COVID-19?The Biochemical journal · 2022Review
Corrections and comments
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Authors and funding
26 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils help to clear pathogens and cellular debris, but can also cause collateral damage within inflamed tissues. Prolonged neutrophil residency within an inflammatory niche can exacerbate tissue pathology. Using both genetic and pharmacological approaches, we show that BCL-XL is required for the persistence of neutrophils within inflammatory sites in mice. We demonstrate that a selective BCL-XL inhibitor (A-1331852) has therapeutic potential by causing apoptosis in inflammatory human neutrophils ex vivo. Moreover, in murine models of acute and chronic inflammatory disease, it reduced inflammatory neutrophil numbers and ameliorated tissue pathology. In contrast, there was minimal effect on circulating neutrophils. Thus, we show a differential survival requirement in activated neutrophils for BCL-XL and reveal a new therapeutic approach to neutrophil-mediated diseases.
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Registered trials
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