Both multiorgan inflammation and myeloid hyperplasia in RelB-deficient mice are T cell dependent
Abstract
Mice with a targeted disruption of RelB, a member of the Rel/NF-κB family of transcription factors, have multifocal, mixed inflammatory cell infiltration in several organs, myeloid hyperplasia, and splenomegaly due to extramedullary hemopoiesis. To elucidate the cellular requirements for this complex phenotype, we have bred RelB-deficient (RelB^(κO)) animals to two strains of immunodeficient mice, recombinase-activating gene-1-deficient (RAG-1^(κO), lacking B and T cells), and Nur77/N10-transgenic mice (Nur77/N10^(TG), lacking only T cells). We also generated mutant mice deficient in both RelB and the p50 subunit of NF-κB (p50^(κO), multiple defects in B cell function). RelB^(κO)RAG-1^(κO) and RelB^(κO)Nur77/N10^(TG) mice are disease-free, while RelB^(κO)p50^(κO) double-mutant animals develop an even more severe phenotype despite the absence of B cells in the inflammatory infiltrates. Thus, both multiorgan inflammation and myeloid hyperplasia in RelB-deficient mice are T cell dependent, whereas B cells are not crucially involved.
Additional Information
© 1996 The American Association of Immunologists. Received for publication May 23, 1996. Accepted for publication August 6, 1996. We thank Kenneth Class for flow cytometry and Michele French and Sophie Komar for excellent technical assistance. We also thank Daniel Carrasco for valuable comments on this manuscript, James K. Loy for microphotographs, and all of the staff in Veterinary Sciences of Bristol-Myers Squibb. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.Additional details
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