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Article

Paucity of clinical disease despite serological autoimmunity and kidney pathology in lupus-prone New Zealand mixed 2328 mice deficient in BAFF.

Journal of immunology (Baltimore, Md. : 1950) - 15 Aug 2006

Jacob Chaim O, Pricop Luminita, Putterman Chaim, Koss Michael N, Liu Yi, Kollaros Maria, Bixler Sarah A, Ambrose Christine M, Scott Martin L, Stohl William

Abstract excerpt

Constitutive overexpression of B cell-activating factor belonging to the TNF family (BAFF) promotes development of systemic lupus erythematosus (SLE), and treatment of SLE mice with BAFF antagonists ameliorates disease. To determine whether SLE can develop de novo in BAFF-deficient hosts, BAFF-deficient New Zealand Mixed (NZM) 2328 (NZM.Baff(-/-)) mice were generated. In NZM.Baff(-/-) mice, spleen B cells...

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Identifiers

PMID: 16888029
DOI: 10.4049/jimmunol.177.4.2671
PMCID: PMC2896675

Genes

TNF

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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