Source:http://linkedlifedata.com/resource/pubmed/id/10651923
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2000-3-20
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pubmed:abstractText |
Flaky skin (fsn) is an autosomal recessive mutation on mouse chromosome 17 that causes severe anaemia, forestomach papillomatosis and a papulosquamous skin disease that resembles psoriasis in humans. In the present paper, it is reported that fsn causes peripheral lymphadenopathy, CD4/CD8 imbalance and hyperresponsiveness to T cell growth factors. Peripheral lymph nodes (PLN) of adult mutant (fsn/fsn) mice were found to contain almost 10-fold more leucocytes than PLN from phenotypically normal littermates (+/fsn or +/+, hereafter referred to as +/?). Analysis of PLN cells using mAbs and flow cytometry revealed that this predominantly lymphoid hyperplasia was characterized by approximately equivalent increases in the numbers of CD3+ T cells and CD19+ B cells. However, expansion within the T cell compartment was non-random, because fsn/fsn PLN had a considerably reduced ratio of CD4+ to CD8+ T cells (1.08 +/- 0.37) compared to +/? PLN (2.47 +/- 0.44, P < 0.0001). In vitro assays of cellular proliferation in response to T and B cell growth factors showed that fsn/fsn PLN cells were hyperresponsive to IL-2, IL-4 and IL-7 when compared with PLN cells from +/? mice. Studies using mesenteric lymph node and peripheral blood cells showed that hyperresponsive cells are widely distributed in fsn/fsn mice. Experiments in newborn mice showed that the lymphoid disturbances caused by fsn are established at least as early as 2 weeks of age, a time that precedes the onset of the earliest clinical skin lesions. These data implicate a role for the fsn gene product in regulating the size and content of the peripheral lymphoid compartment.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0818-9641
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
78
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5-12
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10651923-Animals,
pubmed-meshheading:10651923-Animals, Newborn,
pubmed-meshheading:10651923-B-Lymphocytes,
pubmed-meshheading:10651923-CD4-CD8 Ratio,
pubmed-meshheading:10651923-Disease Models, Animal,
pubmed-meshheading:10651923-Female,
pubmed-meshheading:10651923-Genes, Recessive,
pubmed-meshheading:10651923-Humans,
pubmed-meshheading:10651923-Lymphatic Diseases,
pubmed-meshheading:10651923-Lymphocyte Activation,
pubmed-meshheading:10651923-Male,
pubmed-meshheading:10651923-Mice,
pubmed-meshheading:10651923-Mice, Inbred BALB C,
pubmed-meshheading:10651923-Mice, Mutant Strains,
pubmed-meshheading:10651923-Phenotype,
pubmed-meshheading:10651923-Psoriasis
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pubmed:year |
2000
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pubmed:articleTitle |
The peripheral lymphoid compartment is disrupted in flaky skin mice.
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pubmed:affiliation |
Genesis Research and Development Corporation Limited, Auckland, New Zealand. n.abernethy@genesis.co.nz
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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