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In these mice, the insertion of a retrotransposon in the 3' untranslated region of <jats:italic>Tnf<\/jats:italic> causes a large increase in the expression of the cytokine. We have found that these mice also develop inducible bronchus\u2010associated lymphoid tissue (<jats:styled-content style=\"fixed-case\">iBALT<\/jats:styled-content>), as well as nodular lymphoid hyperplasia (<jats:styled-content style=\"fixed-case\">NLH<\/jats:styled-content>) in the bone marrow. Loss of <jats:styled-content style=\"fixed-case\">TNFR<\/jats:styled-content>1 prevents the development of both types of follicles, but deficiency of <jats:styled-content style=\"fixed-case\">TNFR<\/jats:styled-content>1 in the hematopoietic compartment only prevents the <jats:styled-content style=\"fixed-case\">iBALT<\/jats:styled-content> and not the <jats:styled-content style=\"fixed-case\">NLH<\/jats:styled-content> 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 <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 or <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201023 limits <jats:styled-content style=\"fixed-case\">iBALT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NLH<\/jats:styled-content> development to some extent, it has no effect on polyarthritis or heart valve disease in <jats:styled-content style=\"fixed-case\">BPSM<\/jats:styled-content>1 mice.<\/jats:p>","DOI":"10.1111\/imcb.12197","type":"journal-article","created":{"date-parts":[[2018,8,14]],"date-time":"2018-08-14T16:49:17Z","timestamp":1534265357000},"page":"29-38","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Constitutive overexpression of TNF in BPSM1 mice causes iBALT and bone marrow nodular lymphocytic 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