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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-9-3
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1042-8194
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1367-78
pubmed:dateRevised
2006-11-15
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
pubmed:year
2003
pubmed:articleTitle
Differential chemokine, chemokine receptor and cytokine expression in Epstein-Barr virus-associated lymphoproliferative diseases.
pubmed:affiliation
Department of Pathology, School of Medicine, Fukuoka University, Nanakuma 7-45-1, Jonan-ku, Fukuoka 814-01, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't