Abstract
RelB, a member of the NF-kappa B/Rel family of transcription factors, has been implicated in the constitutive expression of kappa B-regulated genes in lymphoid tissues. We have generated mice carrying a germline mutation of the relB gene, resulting in the absence of RelB protein and a dramatic reduction of constitutive kappa B-binding activity in thymus and spleen. Mice homozygous for the disrupted relB locus had phenotypic abnormalities including multifocal, mixed inflammatory cell infiltration in several organs, myeloid hyperplasia, splenomegaly due to extramedullary hematopoiesis, and a reduced population of thymic dendritic cells. RelB-deficient animals also had an impaired cellular immunity, as observed in contact sensitivity experiments. Thus, RelB plays a decisive role in the hematopoietic system, and its absence cannot be functionally compensated by any other member of the NF-kappa B/Rel family.
MeSH terms
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Aging / immunology*
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Animals
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Blastocyst / physiology
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Bone Marrow / growth & development
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Bone Marrow / pathology
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Bone Marrow / physiology
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Exons
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Female
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Flow Cytometry
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Hematopoiesis / genetics*
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Immunity, Cellular
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Inflammation
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Introns
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Liver / growth & development
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Liver / pathology
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Liver / physiology
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Lung / growth & development
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Lung / pathology
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Lung / physiology
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Lymph Nodes / growth & development
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Lymph Nodes / pathology
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Lymph Nodes / physiology
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Inbred ICR
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Mice, Mutant Strains
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Mice, Transgenic
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NF-kappa B / biosynthesis*
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NF-kappa B / metabolism
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Proto-Oncogene Proteins*
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Spleen / growth & development
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Spleen / pathology
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Spleen / physiology
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Stem Cells / physiology
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Transcription Factor RelB
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Transcription Factors / biosynthesis*
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Transcription Factors / genetics*
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Transfection
Substances
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NF-kappa B
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Proto-Oncogene Proteins
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Relb protein, mouse
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Transcription Factors
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Transcription Factor RelB