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Constitutive overexpression of TNF in BPSM1 mice causes iBALT and bone marrow nodular lymphocytic hyperplasia
Author(s) -
Seillet Cyril,
Arvell Elyas H,
Lacey Derek,
Stutz Michael D,
Pellegrini Marc,
Whitehead Lachlan,
Rimes Joel,
Hawkins Edwin D,
Roediger Ben,
Belz Gabrielle T,
Bouillet Philippe
Publication year - 2019
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/imcb.12197
Subject(s) - bone marrow , tumor necrosis factor alpha , polyarthritis , hyperplasia , pathology , cytokine , biology , medicine , immunology , arthritis
BPSM 1 (Bone phenotype spontaneous mutant 1) mice develop severe polyarthritis and heart valve disease as a result of a spontaneous mutation in the Tnf gene. In these mice, the insertion of a retrotransposon in the 3' untranslated region of Tnf causes a large increase in the expression of the cytokine. We have found that these mice also develop inducible bronchus‐associated lymphoid tissue ( iBALT ), as well as nodular lymphoid hyperplasia ( NLH ) in the bone marrow. Loss of TNFR 1 prevents the development of both types of follicles, but deficiency of TNFR 1 in the hematopoietic compartment only prevents the iBALT and not the NLH phenotype. We show that the development of arthritis and heart valve disease does not depend on the presence of the tertiary lymphoid tissues. Interestingly, while loss of IL ‐17 or IL ‐23 limits iBALT and NLH development to some extent, it has no effect on polyarthritis or heart valve disease in BPSM 1 mice.