pubmed-article:9053444 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9053444 | lifeskim:mentions | umls-concept:C0025927 | lld:lifeskim |
pubmed-article:9053444 | lifeskim:mentions | umls-concept:C0017263 | lld:lifeskim |
pubmed-article:9053444 | lifeskim:mentions | umls-concept:C1423842 | lld:lifeskim |
pubmed-article:9053444 | lifeskim:mentions | umls-concept:C1327413 | lld:lifeskim |
pubmed-article:9053444 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
pubmed-article:9053444 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
pubmed-article:9053444 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:9053444 | pubmed:dateCreated | 1997-3-13 | lld:pubmed |
pubmed-article:9053444 | pubmed:abstractText | Development of T helper cell (Th)1 or Th2 cytokine responses is essential for effector and regulatory functions of T helper cells. We have compared cytokine profiles of myelin basic protein (MBP) Ac1-16 peptide-specific T helper cells from inbred mouse strains expressing identical k haplotype-derived MHC class II molecules B10.A and B10.BR, B10.BR T cell lines (TCL) produced Th1 cytokines (including high levels of TNF-alpha) and induced experimental autoimmune encephalomyelitis after adoptive transfer. In contrast, B10.A TCL produced Th2 cytokines (including low levels of TNF-alpha) and were poorly encephalitogenic. The contributions of the genetic origin of the T cells and the APC were explored. Serial restimulations of the B10.BR TCL with B10.A or (B10.A x B10.BR) F1 splenic antigen presenting cells (APC) during the establishment of TCL markedly reduced both Th1 cytokine production and encephalitogenicity. In addition, a single restimulation with B10. A splenic APC reduced IFN-gamma and TNF-alpha production by established Th1 MBP-specific Ak-restricted B10.BR TCL and by a Th1 KLH-specific, Ek-restricted B10.BR T cell clone. These studies suggest that B10.A and B10.BR APC differ in their ability to stimulate IFN-gamma and TNF-alpha production by mature Th1 cells and also influence their Th1/Th2 commitment in vivo. The nature of the downregulatory activity of B10.A APC on IFN-gamma and TNF-alpha production was explored. 2-hour supernatants from antigen-activated B10.A APC/TCL cultures or from B10.A APC activated by LPS had the same inhibitory effects on IFN-gamma and TNF-alpha production by B10.BR TCL. The downregulatory effects of B10.A APC are independent of TNF-alpha, IL-4, IL-10, IL-12p40, IFN-gamma, IL-13, TGF-beta, and PGE2. Thus, genetic difference(s) between B10.A and B10.BR APC appear(s) to control the production or activity of a novel soluble cytokine regulatory factor that influences Th1/Th2 commitment and controls production of IFN-gamma and TNF-alpha by mature Th1 cells. | lld:pubmed |
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pubmed-article:9053444 | pubmed:language | eng | lld:pubmed |
pubmed-article:9053444 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9053444 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9053444 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9053444 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9053444 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9053444 | pubmed:month | Feb | lld:pubmed |
pubmed-article:9053444 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:9053444 | pubmed:author | pubmed-author:MooreT ATA | lld:pubmed |
pubmed-article:9053444 | pubmed:author | pubmed-author:JonesP PPP | lld:pubmed |
pubmed-article:9053444 | pubmed:author | pubmed-author:UmetsuD TDT | lld:pubmed |
pubmed-article:9053444 | pubmed:author | pubmed-author:DeKruyffR HRH | lld:pubmed |
pubmed-article:9053444 | pubmed:author | pubmed-author:TateK MKM | lld:pubmed |
pubmed-article:9053444 | pubmed:author | pubmed-author:RhaH YHY | lld:pubmed |
pubmed-article:9053444 | pubmed:author | pubmed-author:ConboyI MIM | lld:pubmed |
pubmed-article:9053444 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9053444 | pubmed:day | 3 | lld:pubmed |
pubmed-article:9053444 | pubmed:volume | 185 | lld:pubmed |