Linked Life Data

21148041

Source:http://linkedlifedata.com/resource/pubmed/id/21148041

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-1-6
pubmed:abstractText
Overexpression of the T cell cytokine IL-22 is linked to the development of some chronic diseases, but little is known about IL-22 deficiency in humans. As demonstrated in this study, acne inversa (AI; also designated as Hidradenitis suppurativa) lesions show a relative deficiency of IL-22 and IL-20, but not of IL-17A, IL-26, IFN-?, IL-24, or IL-1?. Moreover, AI lesions had reduced expression of membranous IL-22 and IL-20 receptors and increased expression of the natural IL-22 inhibitor, IL-22 binding protein. AI is a chronic inflammatory skin disease with prevalence up to 4% of the population and in which cutaneous bacterial persistence represents an important pathogenetic factor. Accordingly, we also found a relative deficiency of antimicrobial proteins (AMPs) in AI lesions and a positive correlation between lesional IL-22 and IL-20 versus AMP levels. IL-22, like its tissue cell downstream mediator IL-20, upregulated AMPs in reconstituted human epidermis and was critical for increased AMP levels under inflammatory conditions. The relative IL-22 deficiency in AI was not linked to lesional T cell numbers or Th22/Th1/Th17 subset markers and -inducing cytokines. However, IL-10 was highly expressed in AI lesions and correlated negatively with IL-22 expression. Moreover, IL-10 inhibited IL-22 but not IL-17 production in vitro. The IL-10 overexpression, in turn, was not associated with an elevated presence of regulatory T cells but with the enhanced presence of an IL-10-inducing cytokine. We conclude that IL-22 deficiency may contribute to the pathogenesis of certain chronic disorders as postulated in this paper for AI.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
186
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1228-39
pubmed:meshHeading
pubmed-meshheading:21148041-Adolescent, pubmed-meshheading:21148041-Adult, pubmed-meshheading:21148041-Aged, pubmed-meshheading:21148041-Animals, pubmed-meshheading:21148041-Antimicrobial Cationic Peptides, pubmed-meshheading:21148041-Cells, Cultured, pubmed-meshheading:21148041-Chronic Disease, pubmed-meshheading:21148041-Cytokines, pubmed-meshheading:21148041-Female, pubmed-meshheading:21148041-Hidradenitis Suppurativa, pubmed-meshheading:21148041-Humans, pubmed-meshheading:21148041-Inflammation, pubmed-meshheading:21148041-Inflammation Mediators, pubmed-meshheading:21148041-Interleukins, pubmed-meshheading:21148041-Male, pubmed-meshheading:21148041-Mice, pubmed-meshheading:21148041-Mice, Inbred BALB C, pubmed-meshheading:21148041-Middle Aged, pubmed-meshheading:21148041-Up-Regulation, pubmed-meshheading:21148041-Young Adult
pubmed:year
2011
pubmed:articleTitle
Deficiency of IL-22 contributes to a chronic inflammatory disease: pathogenetic mechanisms in acne inversa.
pubmed:affiliation
Interdisciplinary Group of Molecular Immunopathology, Dermatology/Medical Immunology, University Hospital Charité, D-10117 Berlin, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't