Linked Life Data

11544344

Source:http://linkedlifedata.com/resource/pubmed/id/11544344

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-9-6
pubmed:abstractText
IL-10 is a pleiotropic cytokine with stimulatory and inhibitory properties, and is thought to have a protective role in rheumatoid arthritis and collagen-induced arthritis (CIA). In this study, we investigated how IL-10 deficiency affects CIA and anti-collagen type II (CII) Ab-transferred arthritis in C57BL/10.Q (B10.Q) mice. The B10.Q.IL-10(-/-) mice had an 8-cM 129/Ola fragment around the IL-10 gene. The mice were treated with antibiotics, appeared healthy, and had no colitis. T cells from IL-10(-/-) mice expressed similar levels of IFN-gamma, IL-2, and IL-4 after mitogen stimulation; however, macrophages showed a reduced TNF-alpha production compared with IL-10(+/-) littermates. IL-10(-/-) mice had an increased incidence, and a more severe CIA disease than the IL-10(+/-) littermates. To study the role of IL-10 in T cell tolerance, IL-10(-/-) were crossed into mice carrying the immunodominant epitope, CII(256-270), in cartilage (MMC) or in skin (TSC). Both IL-10(-/-) and IL-10(+/-) MMC and TSC mice were completely tolerized against CIA, indicating that lack of IL-10 in this context did not break tolerance. To investigate whether IL-10 was important in the effector phase of CIA, arthritis was induced with anti-CII Abs. Surprisingly, IL-10(-/-) were less susceptible to Ab-transferred arthritis, as only 30% showed signs of disease compared with 90% of the littermates. Therefore, IL-10 seemed to have a protective role in CIA, but seemed to exacerbate the arthritogenicity of anti-CII Abs. These data emphasize the importance of studying IL-10 in a defined genetic context in vivo, to understand its role in a complex disease like arthritis.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
167
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3505-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11544344-Animals, pubmed-meshheading:11544344-Antibodies, Monoclonal, pubmed-meshheading:11544344-Arthritis, pubmed-meshheading:11544344-Arthritis, Experimental, pubmed-meshheading:11544344-Autoimmune Diseases, pubmed-meshheading:11544344-Colitis, pubmed-meshheading:11544344-Collagen Type II, pubmed-meshheading:11544344-Cytokines, pubmed-meshheading:11544344-Disease Models, Animal, pubmed-meshheading:11544344-Genotype, pubmed-meshheading:11544344-Immune Tolerance, pubmed-meshheading:11544344-Immunization, pubmed-meshheading:11544344-Immunization, Passive, pubmed-meshheading:11544344-Immunodominant Epitopes, pubmed-meshheading:11544344-Interleukin-10, pubmed-meshheading:11544344-Macrophages, pubmed-meshheading:11544344-Male, pubmed-meshheading:11544344-Mice, pubmed-meshheading:11544344-Mice, Inbred C57BL, pubmed-meshheading:11544344-Mice, Knockout, pubmed-meshheading:11544344-Mice, Transgenic, pubmed-meshheading:11544344-Specific Pathogen-Free Organisms, pubmed-meshheading:11544344-Tumor Necrosis Factor-alpha
pubmed:year
2001
pubmed:articleTitle
IL-10-deficient B10.Q mice develop more severe collagen-induced arthritis, but are protected from arthritis induced with anti-type II collagen antibodies.
pubmed:affiliation
Section for Medical Inflammation Research, University of Lund, Lund, Sweden. Asa.Johansson@inflam.lu.se
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't