Abstract
The murine X-linked lymphoproliferative disease scurfy is similar to the Wiskott-Aldrich syndrome in humans. Disease in scurfy (sf) mice is mediated by CD4+ T cells. Based on similarities in scurfy mice and transgenic mice that overexpress specific cytokine genes, we evaluated the expression of cytokines in the lesions of sf mice by Northern blotting, quantitative reverse-transcription polymerase chain reaction (RT-PCR) and by hybridization in situ. Overall, the phenotypic characteristics of scurfy disease correlated well with increased interleukin (IL)-4 (lymphadenopathy), IL-6 (B cell proliferation, hypergammaglobulinemia), IL-7 (dermal inflammatory cell infiltration), and high levels of tumor necrosis factor-alpha (wasting).
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Base Sequence
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Blotting, Northern
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Cytokines / biosynthesis*
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Cytokines / genetics*
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Disease Models, Animal
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Gene Expression Regulation / immunology
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Interleukin-4 / biosynthesis
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Interleukin-4 / genetics
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Interleukin-6 / biosynthesis
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Interleukin-6 / genetics
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Interleukin-7 / biosynthesis
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Interleukin-7 / genetics
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Male
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Mice
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Mice, Mutant Strains
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Molecular Sequence Data
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Polymerase Chain Reaction
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T-Lymphocytes / metabolism
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Transcription, Genetic / immunology
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Wiskott-Aldrich Syndrome / genetics*
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Wiskott-Aldrich Syndrome / immunology
Substances
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Cytokines
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Interleukin-6
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Interleukin-7
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Interleukin-4