Source:http://linkedlifedata.com/resource/pubmed/id/12624779
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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0002171,
umls-concept:C0017262,
umls-concept:C0019764,
umls-concept:C0063695,
umls-concept:C0185117,
umls-concept:C0301896,
umls-concept:C0332120,
umls-concept:C0439851,
umls-concept:C0442821,
umls-concept:C1539081,
umls-concept:C1552596,
umls-concept:C1710548,
umls-concept:C1947931,
umls-concept:C2348519,
umls-concept:C2911684
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pubmed:issue |
12
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pubmed:dateCreated |
2003-3-7
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pubmed:abstractText |
The pathological role played by T cells infiltrating hair follicles in lesions of alopecia areata (AA) is unknown. We examined the expression in cryostat sections of scalp skin obtained from a total of 28 patients with AA and from five normal control subjects of (1) molecules related to the induction of cell death including Fas, Fas ligand (FasL), perforin, granzyme B (GB), and TIA-1, (2) molecules related to antigen presentation including CD1a, CD40, CD54, CD80, and CD86, and (3) molecules induced by interferon gamma (IFN-gamma) including CD40, CD54, Fas, and HLA-DR. CD3(+) T cells infiltrated perifollicularly, perivascularly and in the hair structure and there was a predominance of CD4(+) over CD8(+) cells. Antigen-presenting cells expressing CD1a, CD40, CD54, or HLA-DR were also seen. Expression of CD40, CD54, HLA-DR and CD95 was also seen in the hair structure including the dermal papilla. Consistent with these observations, IFN-gamma-producing cells were also detected in the perifollicular infiltrate. In contrast, few Fas-L(+), perforin(+), GB(+) or TIA-1(+) cells were found adjacent to the follicles. Apoptotic cells were recognized only in the outer root sheath of catagen hairs. These findings suggest that infiltrating T cells interact with perifollicular or follicular antigen-presenting cells to produce IFN-gamma, which deprives dermal papilla cells of their ability to maintain anagen hair growth.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0340-3696
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
294
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
536-43
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12624779-Adolescent,
pubmed-meshheading:12624779-Adult,
pubmed-meshheading:12624779-Alopecia Areata,
pubmed-meshheading:12624779-Antigen-Presenting Cells,
pubmed-meshheading:12624779-Antigens, CD40,
pubmed-meshheading:12624779-Apoptosis,
pubmed-meshheading:12624779-Case-Control Studies,
pubmed-meshheading:12624779-Child,
pubmed-meshheading:12624779-Cytotoxicity, Immunologic,
pubmed-meshheading:12624779-Female,
pubmed-meshheading:12624779-HLA-DR Antigens,
pubmed-meshheading:12624779-Hair,
pubmed-meshheading:12624779-Humans,
pubmed-meshheading:12624779-Intercellular Adhesion Molecule-1,
pubmed-meshheading:12624779-Interferon-gamma,
pubmed-meshheading:12624779-Lymphocyte Activation,
pubmed-meshheading:12624779-Male,
pubmed-meshheading:12624779-Middle Aged,
pubmed-meshheading:12624779-T-Lymphocyte Subsets
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pubmed:year |
2003
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pubmed:articleTitle |
Strong expression of CD40, CD54 and HLA-DR antigen and lack of evidence for direct cellular cytotoxicity are unique immunohistopathological features in alopecia areata.
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pubmed:affiliation |
Department of Dermatology, Tohoku University School of Medicine, l-l Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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