pubmed-article:11238667 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C0008109 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C0282641 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C0206552 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C1173313 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C0971858 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C1149207 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:11238667 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
pubmed-article:11238667 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:11238667 | pubmed:dateCreated | 2001-3-12 | lld:pubmed |
pubmed-article:11238667 | pubmed:abstractText | Chronic inflammatory autoimmune diseases such as diabetes, experimental autoimmune encephalomyelitis, and collagen-induced arthritis (CIA) are associated with type 1 (Th1, Tc1) T cell-dependent responses against autoantigens. Immune deviation toward type 2 (Th2, Tc2) response has been proposed as a potential means of gene therapy or immunomodulation to treat autoimmune diseases based on evidence that type 2 cytokines can prevent or alleviate these conditions. In this report we assessed the effects of elevated type 2 responses on CIA using transgenic mice expressing an IL-2R beta/IL-4R alpha chimeric cytokine receptor transgene specifically in T cells. In response to IL-2 binding, this chimeric receptor transduces IL-4-specific signals and dramatically enhances type 2 responses. In contrast to published reports of Th2-mediated protection, CIA was exacerbated in IL-2R beta/IL-4R alpha chimeric receptor transgenic mice, with increased disease incidence, severity, and earlier disease onset. The aggravated disease in transgenic mice was associated with an increase in type 2 cytokines (IL-4, IL-5, IL-10) and an increase in collagen-specific IgG1 levels. However, IFN-gamma production is not affected significantly in the induction phase of the disease. There is also an extensive eosinophilic infiltration in the arthritic joints of the transgenic animal, suggesting a direct contribution of type 2 response to joint inflammation. Taken together, our findings provide novel evidence that enhancement of a polyclonal type 2 response in immunocompetent hosts may exacerbate an autoimmune disease such as CIA, rather than serving a protective role. This finding raises significant caution with regard to the potential use of therapeutic approaches based on immune deviation toward type 2 responses. | lld:pubmed |
pubmed-article:11238667 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:language | eng | lld:pubmed |
pubmed-article:11238667 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:11238667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11238667 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11238667 | pubmed:month | Mar | lld:pubmed |
pubmed-article:11238667 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:11238667 | pubmed:author | pubmed-author:ChenYY | lld:pubmed |
pubmed-article:11238667 | pubmed:author | pubmed-author:ChenJJ | lld:pubmed |
pubmed-article:11238667 | pubmed:author | pubmed-author:BoothbyMM | lld:pubmed |
pubmed-article:11238667 | pubmed:author | pubmed-author:GoralM IMI | lld:pubmed |
pubmed-article:11238667 | pubmed:author | pubmed-author:RosloniecEE | lld:pubmed |
pubmed-article:11238667 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11238667 | pubmed:day | 15 | lld:pubmed |
pubmed-article:11238667 | pubmed:volume | 166 | lld:pubmed |
pubmed-article:11238667 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11238667 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11238667 | pubmed:pagination | 4163-9 | lld:pubmed |
pubmed-article:11238667 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:11238667 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11238667 | pubmed:articleTitle | Redirection of T cell effector function in vivo and enhanced collagen-induced arthritis mediated by an IL-2R beta/IL-4R alpha chimeric cytokine receptor transgene. | lld:pubmed |
pubmed-article:11238667 | pubmed:affiliation | Division of Rheumatology, Department of Medicine, Vanderbilt University Medical School, Nashville, TN 37232, USA. | lld:pubmed |
pubmed-article:11238667 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11238667 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:11238667 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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