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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-8-26
pubmed:abstractText
Eosinophils participate in allergic inflammation, where expression of T helper cell type 2 (Th2) cytokines such as interleukin (IL)-4 and IL-5 are seen. However, eosinophils sometimes accumulate during disease with expression of Th1 cytokines [i.e., interferon-gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and IL-1beta]. In this study, we investigated whether eosinophils can respond with expression of the IFN-inducible C-X-C chemokines monokine induced by IFN-gamma [MIG; CXC chemokine ligand 9 (CXCL9)], IFN-gamma-inducible protein (IP-10/CXCL10), and IFN-inducible T cell alpha chemoattractant (I-TAC/CXCL11). These chemokines share the ability to recruit and activate T cells and natural killer cells to sites of inflammation. We found that IFN-gamma induced rapid and sustained gene expression of MIG, IP-10, and I-TAC in eosinophils, as detected by quantitative reverse transcriptase-polymerase chain reaction. During incubation, IFN-gamma-stimulated eosinophils released MIG and IP-10, as detected by enzyme-linked immunosorbent assay, while I-TAC could not be detected in the medium. TNF-alpha but not IL-1beta enhanced the IFN-gamma-induced production of MIG and IP-10. Conversely, addition of the Th2 cytokine IL-4 down-regulated IFN-gamma-induced synthesis of MIG and IP-10 in eosinophils. Crohn's disease is characterized by a Th1-polarized inflammation and presence of eosinophils. In lesions from this disease, MIG was detected in eosinophils by immunohistochemistry. Taken together, the results point to immunoregulatory roles for eosinophils during some diseases with Th1-polarized inflammation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0741-5400
pubmed:author
pubmed:issnType
Print
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
685-91
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15197236-Cell Line, pubmed-meshheading:15197236-Chemokine CXCL10, pubmed-meshheading:15197236-Chemokine CXCL11, pubmed-meshheading:15197236-Chemokine CXCL9, pubmed-meshheading:15197236-Chemokines, CXC, pubmed-meshheading:15197236-Chemotaxis, Leukocyte, pubmed-meshheading:15197236-Crohn Disease, pubmed-meshheading:15197236-Dose-Response Relationship, Drug, pubmed-meshheading:15197236-Down-Regulation, pubmed-meshheading:15197236-Drug Synergism, pubmed-meshheading:15197236-Eosinophils, pubmed-meshheading:15197236-Gene Expression Regulation, pubmed-meshheading:15197236-Humans, pubmed-meshheading:15197236-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:15197236-Interferon-gamma, pubmed-meshheading:15197236-Interleukin-4, pubmed-meshheading:15197236-RNA, Messenger, pubmed-meshheading:15197236-T-Lymphocytes, pubmed-meshheading:15197236-Th1 Cells, pubmed-meshheading:15197236-Tumor Necrosis Factor-alpha
pubmed:year
2004
pubmed:articleTitle
Human eosinophils produce the T cell-attracting chemokines MIG and IP-10 upon stimulation with IFN-gamma.
pubmed:affiliation
Department of Medical Microbiology, Malmö University Hospital, Tornavägen 10, SE-221 84 Lund, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't