Linked Life Data

10640777

Source:http://linkedlifedata.com/resource/pubmed/id/10640777

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-2-24
pubmed:abstractText
Viral IL-10 (vIL-10) and soluble TNF receptor (sTNFR) are anti-inflammatory proteins that can suppress collagen-induced arthritis (CIA). These and related proteins have shown efficacy in the treatment of human rheumatoid arthritis; however, neither alone is able to completely suppress disease. Furthermore, they have short half-lives, necessitating frequent administration. To determine the ability of these proteins to act synergistically following gene transfer, arthritis was induced in DBA/1 male mice by immunization with type II collagen on days 0 and 21. Mice were injected i.v. either before disease onset (day 20) or after disease onset (day 28) with 1010 particles of adenovirus encoding vIL-10, a soluble TNF receptor-IgG1 fusion protein (sTNFR-Ig), a combination of both vectors, or a control vector lacking a transgene. Significant synergism was observed with the combination of vIL-10 and sTNFR-Ig, with a substantial reduction in both the incidence and severity of disease as well as inhibition of progression of established disease. sTNFR-Ig alone had no effect on CIA. vIL-10 alone inhibited disease when given before disease onset, but had minimal effect on established disease. Both proteins inhibited spleen cell proliferation and IFN-gamma secretion in response to stimulation with type II collagen, but only vIL-10 reduced the synovial mRNA levels of the proinflammatory cytokines IL-1beta, TNF-alpha, and IL-6. These findings demonstrate that vIL-10 and sTNFR-Ig act synergistically in suppressing CIA and suggest that gene transfer offers a potential therapeutic modality for the treatment of arthritis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
164
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1576-81
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10640777-Adenoviridae, pubmed-meshheading:10640777-Animals, pubmed-meshheading:10640777-Arthritis, Experimental, pubmed-meshheading:10640777-B-Lymphocytes, pubmed-meshheading:10640777-Collagen, pubmed-meshheading:10640777-Cytokines, pubmed-meshheading:10640777-Drug Synergism, pubmed-meshheading:10640777-Gene Transfer Techniques, pubmed-meshheading:10640777-Genetic Vectors, pubmed-meshheading:10640777-Hindlimb, pubmed-meshheading:10640777-Humans, pubmed-meshheading:10640777-Immunoglobulin G, pubmed-meshheading:10640777-Interleukin-10, pubmed-meshheading:10640777-Lymphocyte Activation, pubmed-meshheading:10640777-Male, pubmed-meshheading:10640777-Mice, pubmed-meshheading:10640777-Mice, Inbred DBA, pubmed-meshheading:10640777-RNA, Messenger, pubmed-meshheading:10640777-Receptors, Tumor Necrosis Factor, pubmed-meshheading:10640777-Solubility, pubmed-meshheading:10640777-T-Lymphocytes, pubmed-meshheading:10640777-Viral Proteins
pubmed:year
2000
pubmed:articleTitle
Viral IL-10 and soluble TNF receptor act synergistically to inhibit collagen-induced arthritis following adenovirus-mediated gene transfer.
pubmed:affiliation
William S. Rowe Division of Rheumatology, Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't