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Article

Defective regulation of CXCR2 facilitates neutrophil release from bone marrow causing spontaneous inflammation in severely NF-kappa B-deficient mice.

Journal of immunology (Baltimore, Md. : 1950) - 1 Jul 2010

von Vietinghoff Sibylle, Asagiri Masataka, Azar David, Hoffmann Alexander, Ley Klaus

Abstract excerpt

NF-kappaB is a major regulator of innate and adaptive immunity. Neutrophilic granulocytes (neutrophils) constitutively express RelA/p65 (Rela), c-Rel (Crel), and p50 (Nfkappab1) but not p52 (Nfkappab2) subunits. In this paper, we describe Crel(-/-)Nfkappab1(-/-)Rela(+/-) mice that have the most severe genetic neutrophil NF-kappaB deficiency compatible with life, Rela(-/-) mice being embryonic lethal....

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Source

Open in PubMed Open full text

Identifiers

PMID: 20519647
DOI: 10.4049/jimmunol.1000339
PMCID: PMC2891140

Genes

CXCR2
CXCL1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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