Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-4-28
pubmed:abstractText
IL-19, IL-20, IL-22, IL-24, IL-26, IL-28, and IL-29 are new members of the IL-10 interferon family. Monocytes are well-known sources of IL-19, IL-20, and IL-24. We demonstrated here that monocytes also expressed IL-29, and monocyte differentiation into macrophages (Mphi) or dendritic cells (DCs) strongly changed their production capacity of these cytokines. Maturation of DCs with bacterial stimuli induced high expression of IL-28/IL-29 and IL-20. Simulated T cell interaction and inflammatory cytokines induced IL-29 and IL-20 in maturing DCs, respectively. Compared with monocytes, DCs expressed only minimal IL-19 levels and no IL-24. The differentiation of monocytes into Mphi reduced their IL-19 and terminated their IL-20, IL-24, and IL-29 production capacity. Like monocytes, neither Mphi nor DCs expressed IL-22 or IL-26. The importance of maturing DCs as a source of IL-28/IL-29 was supported by the much higher mRNA levels of these mediators in maturing DCs compared with those in CMV-infected fibroblasts, and the presence of IL-28 in lymph nodes but not in liver of lipopolysaccharide-injected mice. IL-19, IL-20, IL-22, IL-24, and IL-26 do not seem to affect Mphi or DCs as deduced from the lack of corresponding receptor chains. The significance of IL-20 and IL-28/IL-29 coexpression in maturing DCs may lie in the broadly amplified innate immunity in neighboring tissue cells like keratinocytes. In fact, IL-20 induced the expression of antimicrobial proteins, whereas IL-28/IL-29 enhanced the expression of toll-like receptors (TLRs) and the response to TLR ligands. However, the strongest response to TLR2 and TLR3 activation showed keratinocytes in the simultaneous presence of IL-20 and IL-29.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0741-5400
pubmed:author
pubmed:issnType
Print
pubmed:volume
83
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1181-93
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:18281438-Animals, pubmed-meshheading:18281438-CD4-Positive T-Lymphocytes, pubmed-meshheading:18281438-Cell Differentiation, pubmed-meshheading:18281438-Cells, Cultured, pubmed-meshheading:18281438-Child, pubmed-meshheading:18281438-Chondrocytes, pubmed-meshheading:18281438-Dendritic Cells, pubmed-meshheading:18281438-Humans, pubmed-meshheading:18281438-Immunity, Innate, pubmed-meshheading:18281438-Interleukins, pubmed-meshheading:18281438-Keratinocytes, pubmed-meshheading:18281438-Lipopolysaccharides, pubmed-meshheading:18281438-Mice, pubmed-meshheading:18281438-Mice, Inbred BALB C, pubmed-meshheading:18281438-Monocytes, pubmed-meshheading:18281438-RNA, Messenger, pubmed-meshheading:18281438-Reference Values, pubmed-meshheading:18281438-Toll-Like Receptor 2, pubmed-meshheading:18281438-Toll-Like Receptor 4
pubmed:year
2008
pubmed:articleTitle
Maturing dendritic cells are an important source of IL-29 and IL-20 that may cooperatively increase the innate immunity of keratinocytes.
pubmed:affiliation
Interdisciplinary Group of Molecular Immunopathology, Dermatology/Medical Immunology, University Hospital Charité, Berlin, Germany. kerstin.wolk@charite.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't