pubmed-article:2295798 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2295798 | lifeskim:mentions | umls-concept:C0026944 | lld:lifeskim |
pubmed-article:2295798 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
pubmed-article:2295798 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
pubmed-article:2295798 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:2295798 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
pubmed-article:2295798 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
pubmed-article:2295798 | lifeskim:mentions | umls-concept:C0443211 | lld:lifeskim |
pubmed-article:2295798 | lifeskim:mentions | umls-concept:C1524063 | lld:lifeskim |
pubmed-article:2295798 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
pubmed-article:2295798 | lifeskim:mentions | umls-concept:C0067015 | lld:lifeskim |
pubmed-article:2295798 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:2295798 | pubmed:dateCreated | 1990-2-9 | lld:pubmed |
pubmed-article:2295798 | pubmed:abstractText | Mycoplasma arthritidis produces a soluble protein which is active for murine and human lymphocytes when presented by Ia-bearing accessory cells. By using fibroblasts transfected in vitro with various class II Ag, we demonstrated that presentation of the M. arthritidis mitogen (MAM) to T cells was mediated by E alpha-containing molecules. We also showed that splenocytes from transgenic mice expressing E alpha heterozygously (B10.TRG E alpha+) or homozygously (B10.E alpha TG +/+) underwent a similar proliferation in response to MAM as compared with the failure of control B10.TRG E alpha- splenocytes to respond to MAM. Although splenocytes from inbred C3H and CBA mice exhibited much higher proliferative responses to MAM than did those from B10.TRG.E alpha+ or B10.E alpha TG +/+ mice, flow cytometry showed similar levels of E alpha expression. Furthermore, gamma-irradiated splenocytes from B10.TRG E alpha + mice presented MAM to T hybridoma cells with a similar efficacy as did splenocytes from C3H mice. The lesser response to MAM of lymphocytes from the E alpha transgenic mice as compared with those from C3H and B10.K mice was likewise not due to differential expression of their V beta TCR. We conclude that presentation of MAM to T cells is accomplished by E alpha-containing molecules. The studies also suggest that the conserved, nonpolymorphic regions of class II molecules may play an important role in host immune response to microbial products. | lld:pubmed |
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pubmed-article:2295798 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2295798 | pubmed:language | eng | lld:pubmed |
pubmed-article:2295798 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2295798 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:2295798 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2295798 | pubmed:month | Jan | lld:pubmed |
pubmed-article:2295798 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:2295798 | pubmed:author | pubmed-author:DavidC SCS | lld:pubmed |
pubmed-article:2295798 | pubmed:author | pubmed-author:LynchD HDH | lld:pubmed |
pubmed-article:2295798 | pubmed:author | pubmed-author:ColeB CBC | lld:pubmed |
pubmed-article:2295798 | pubmed:author | pubmed-author:KartchnerD... | lld:pubmed |
pubmed-article:2295798 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2295798 | pubmed:day | 15 | lld:pubmed |
pubmed-article:2295798 | pubmed:volume | 144 | lld:pubmed |
pubmed-article:2295798 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2295798 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2295798 | pubmed:pagination | 420-4 | lld:pubmed |
pubmed-article:2295798 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:2295798 | pubmed:year | 1990 | lld:pubmed |
pubmed-article:2295798 | pubmed:articleTitle | The use of transfected fibroblasts and transgenic mice establishes that stimulation of T cells by the Mycoplasma arthritidis mitogen is mediated by E alpha. | lld:pubmed |
pubmed-article:2295798 | pubmed:affiliation | Department of Internal Medicine, University of Utah College of Medicine, Salt Lake City 84132. | lld:pubmed |
pubmed-article:2295798 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2295798 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:2295798 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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