rdf:type |
|
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0022567,
umls-concept:C0024297,
umls-concept:C0030685,
umls-concept:C0031437,
umls-concept:C0039194,
umls-concept:C0205263,
umls-concept:C0221198,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C1123023,
umls-concept:C1171362,
umls-concept:C1283071,
umls-concept:C1515670,
umls-concept:C1963578
|
pubmed:issue |
3
|
pubmed:dateCreated |
1990-9-20
|
pubmed:abstractText |
UM4D4 (CDw60), the surface molecule of a novel antigen-independent T-cell activation pathway, was found to be highly expressed on lesional psoriatic T cells. To examine whether UM4D4 represents a T-cell activation pathway for psoriatic T cells, a T-cell line was initiated from an acute skin lesion and cloned by limiting dilution. Clonality was verified by analysis of T-cell receptor gene rearrangement. All T-cell clones tested, whether CD4+2H4+CD8-, CD4+2H4-CD8-, or CD4-CD8+CD11b-, expressed UM4D4 and were activated by the monoclonal antibody anti-UM4D4. Lesional psoriatic T-cell clones were heterogeneous in the degree of anti-UM4D4-induced proliferation and in their production of IL-2 and gamma-interferon. Lymphokines released by anti-UM4D4 activation were capable of inducing ICAM-1 and HLA-DR expression on cultured normal keratinocytes. Thus, the high expression of UM4D4 on T-cells in psoriatic skin provides an alternative mechanism for T-cell activation that may be operative in the psoriatic lesional milieu. Indeed, activation of lesional T-cells through the UM4D4 molecule resulted in release of lymphokines that directly induced keratinocytes to express a phenotype displayed in psoriatic skin lesions.
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pubmed:grant |
|
pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/CDw60 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-DR Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphokines
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
|
pubmed:issn |
0022-202X
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
95
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
N
|
pubmed:pagination |
275-82
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:1974570-Antigens, CD,
pubmed-meshheading:1974570-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:1974570-Cell Adhesion Molecules,
pubmed-meshheading:1974570-Clone Cells,
pubmed-meshheading:1974570-HLA-DR Antigens,
pubmed-meshheading:1974570-Humans,
pubmed-meshheading:1974570-Intercellular Adhesion Molecule-1,
pubmed-meshheading:1974570-Interferon-gamma,
pubmed-meshheading:1974570-Interleukin-2,
pubmed-meshheading:1974570-Keratinocytes,
pubmed-meshheading:1974570-Lymphokines,
pubmed-meshheading:1974570-Phenotype,
pubmed-meshheading:1974570-Psoriasis,
pubmed-meshheading:1974570-Skin,
pubmed-meshheading:1974570-T-Lymphocytes
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pubmed:year |
1990
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pubmed:articleTitle |
UM4D4+ (CDw60) T cells are compartmentalized into psoriatic skin and release lymphokines that induce a keratinocyte phenotype expressed in psoriatic lesions.
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pubmed:affiliation |
Department of Dermatology, University of Michigan School of Medicine, Ann Arbor 48109-0530.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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