Source:http://linkedlifedata.com/resource/pubmed/id/12952231
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2003-9-3
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pubmed:abstractText |
T cell immunity plays an important role in the clinicopathology of Epstein-Barr virus (EBV)-associated diseases. Acute EBV-induced infectious mononucleosis (IM) is a common self-limiting disease, however, other EBV-associated diseases, including chronic active EBV infection (CAEBV), NK cell lymphoma (NKL), and Hodgkin's lymphoma (HL), exhibit distinct clinical features. Chemokines are members of a family of small-secreted proteins. The relationships between chemokines and the chemokine receptor (R) are thought to be important for selectivity of local immunity. Some chemokines, chemokine R and cytokines closely associate with the T cell subtypes, Th1 and Th2 T cells and cytotoxic cells. To clarify the role of T cell immunity in EBV-associated diseases, we conducted gene expression profiling, using chemokine, chemokine R and cytokine DNA chips. Compared to EBV negative non-specific lymphadenitis, CAEBV and NKL exhibited diffuse down- and up-regulation, respectively, of these gene profiles. IM had a predominantly Th1-type profile, whereas HL had a mixed Th1/Th2-type profile. Reduction of the Th1-type cytokine interferon gamma (IFN-gamma) in CAEBV was confirmed by Reverse transcriptase-polymerase chain reaction, whereas IFN-gamma expression was markedly enhanced in NKL, and moderately enhanced in IM. Compared to IM, CAEBV showed slight elevation of "regulated upon activation, normal T expressed and secreted" (RANTES), but almost all other genes assayed were down-regulated. NKL exhibited elevated expression of numerous genes, particularly IFN-gamma-inducible-10 (IP-10) and monokine induced by IFN-gamma (MIG). HL showed variable elevated and reduced expression of various genes, with increased expression of IL-13 receptor and MIG. Our study demonstrated the enormous potential of gene expression profiling for clarifying the pathogenesis of EBV-associated diseases.
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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 |
Aug
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pubmed:issn |
1042-8194
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pubmed:author |
pubmed-author:HamasakiMakotoM,
pubmed-author:KarubeKennosukeK,
pubmed-author:KikuchiMasahiroM,
pubmed-author:OhgaShouichiS,
pubmed-author:OhshimaKoichiK,
pubmed-author:SuefujiHiroakiH,
pubmed-author:SuzukiKeikoK,
pubmed-author:SuzumiyaJunjiJ,
pubmed-author:TutiyaTakeshiT,
pubmed-author:YamaguchiTakahiroT
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pubmed:issnType |
Print
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pubmed:volume |
44
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1367-78
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12952231-Adolescent,
pubmed-meshheading:12952231-Adult,
pubmed-meshheading:12952231-Chemokines,
pubmed-meshheading:12952231-Child,
pubmed-meshheading:12952231-Child, Preschool,
pubmed-meshheading:12952231-Cytokines,
pubmed-meshheading:12952231-Epstein-Barr Virus Infections,
pubmed-meshheading:12952231-Female,
pubmed-meshheading:12952231-Gene Expression Profiling,
pubmed-meshheading:12952231-Herpesvirus 4, Human,
pubmed-meshheading:12952231-Humans,
pubmed-meshheading:12952231-Immunity, Cellular,
pubmed-meshheading:12952231-Lymphadenitis,
pubmed-meshheading:12952231-Lymphoproliferative Disorders,
pubmed-meshheading:12952231-Male,
pubmed-meshheading:12952231-Middle Aged,
pubmed-meshheading:12952231-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:12952231-RNA, Messenger,
pubmed-meshheading:12952231-Receptors, Chemokine,
pubmed-meshheading:12952231-T-Lymphocytes,
pubmed-meshheading:12952231-Th1 Cells,
pubmed-meshheading:12952231-Th2 Cells
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pubmed:year |
2003
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pubmed:articleTitle |
Differential chemokine, chemokine receptor and cytokine expression in Epstein-Barr virus-associated lymphoproliferative diseases.
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pubmed:affiliation |
Department of Pathology, School of Medicine, Fukuoka University, Nanakuma 7-45-1, Jonan-ku, Fukuoka 814-01, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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