| pubmed-article:9034138 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9034138 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
| pubmed-article:9034138 | lifeskim:mentions | umls-concept:C1326205 | lld:lifeskim |
| pubmed-article:9034138 | lifeskim:mentions | umls-concept:C0034790 | lld:lifeskim |
| pubmed-article:9034138 | lifeskim:mentions | umls-concept:C0024518 | lld:lifeskim |
| pubmed-article:9034138 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
| pubmed-article:9034138 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:9034138 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:9034138 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:9034138 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:9034138 | lifeskim:mentions | umls-concept:C1510827 | lld:lifeskim |
| pubmed-article:9034138 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:9034138 | pubmed:dateCreated | 1997-3-14 | lld:pubmed |
| pubmed-article:9034138 | pubmed:abstractText | Multiple sclerosis is an autoimmune disease thought to be mediated by CD4+ T helper cells (Th). Experimental autoimmune encephalomyelitis is a rodent model of multiple sclerosis and has been used extensively to explore a variety of immunotherapies using soluble protein or peptide antigens. The underlying mechanisms of such therapy have been attributed to induction of T cell anergy, a switch in Th1 to Th2 responses, or peripheral deletion of autoreactive T cells. In this study, we have developed transgenic mice expressing a T cell receptor (TCR) specific for the NH2-terminal peptide Ac1-11 of the autoantigen myelin basic protein to explore the mechanism of soluble peptide therapy. T cells from these mice are highly skewed toward the CD4 population and have an abnormal thymic architecture, a phenomenon found in other TCR transgenic mice that exhibit a highly skewed CD4/CD8 ratio. Soluble Ac1-11 or the analogues Ac 1-11 [4A] or Ac1-11[4Y] (which bind to the major histocompatibility complex [MHC] class II molecule I-Au with increasing affinities) given intravenously activates T cells, rendering cells hyperresponsive in vitro for at least two days after injection. Concomitantly, T cells apoptose in the periphery, the degree of which correlates with the affinity of the peptide for the MHC. In addition, a shift in the T helper phenotype of the surviving T cells occurs such that the low affinity peptide, Ac1-11, induces primarily a Th1 response, whereas the highest affinity peptide, Ac1-11[4Y], induces primarily a Th2 type response. These data show that both the nature and the presumed number of the peptide-MHC complexes formed during specific peptide therapy affect both the degree of peripheral programmed cell death as well as the outcome of the T helper subset response in vivo, leading to amelioration of disease. | lld:pubmed |
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| pubmed-article:9034138 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9034138 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9034138 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9034138 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9034138 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:9034138 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:9034138 | pubmed:author | pubmed-author:McDevittH OHO | lld:pubmed |
| pubmed-article:9034138 | pubmed:author | pubmed-author:van EwijkWW | lld:pubmed |
| pubmed-article:9034138 | pubmed:author | pubmed-author:PearsonC ICI | lld:pubmed |
| pubmed-article:9034138 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9034138 | pubmed:day | 17 | lld:pubmed |
| pubmed-article:9034138 | pubmed:volume | 185 | lld:pubmed |
| pubmed-article:9034138 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9034138 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9034138 | pubmed:pagination | 583-99 | lld:pubmed |
| pubmed-article:9034138 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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