| pubmed-article:1671004 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1671004 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:1671004 | lifeskim:mentions | umls-concept:C0021758 | lld:lifeskim |
| pubmed-article:1671004 | lifeskim:mentions | umls-concept:C0020846 | lld:lifeskim |
| pubmed-article:1671004 | lifeskim:mentions | umls-concept:C0018133 | lld:lifeskim |
| pubmed-article:1671004 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:1671004 | pubmed:dateCreated | 1991-2-22 | lld:pubmed |
| pubmed-article:1671004 | pubmed:abstractText | Intravenous injection of 2 x 10(8) DBA/2 spleen cells into adult intact (C57BL/6 x DBA/2) F1 mice results in a stimulatory graft-versus-host reaction (GVHR) linked to the recognition by donor CD4+ T cells of Ia alloantigens on host B cells. In the experiments presented here, we found that this GVHR is associated with a major increase in IgE serum levels which was already present 7 days after the cell transfer. At 6 weeks, mean IgE levels were more than 200-fold above the control values. Host B cells were responsible for the hypersecretion of IgE in stimulatory GVHR since it was also observed when the DBA/2 donor inoculum was depleted of B cells but not when the F1 recipients were irradiated. The induction of IgE secretion required donor CD4+ T cells as treatment of the donor inoculum with lytic anti-CD4 monoclonal antibody (MoAb) completely prevented the occurrence of the hyper IgE whereas depletion of CD8+ cells had no influence on this parameter. The role played by interleukin-4 (IL-4) in this model was analysed in vivo by the administration of the 11B11 anti-IL-4 rat MoAb (total dose 36 mg) during the first 12 days following induction of stimulatory GVHR by 8 x 10(7) DBA/2 spleen cells. This treatment completely prevented the development of hyper IgE whereas the administration of a control rat MoAb had no significant effect. We conclude that stimulatory GVHR in mice is associated with a major increase in serum IgE which is mediated by IL-4. | lld:pubmed |
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| pubmed-article:1671004 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1671004 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1671004 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1671004 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:1671004 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1671004 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:1671004 | pubmed:issn | 0009-9104 | lld:pubmed |
| pubmed-article:1671004 | pubmed:author | pubmed-author:GoldmanMM | lld:pubmed |
| pubmed-article:1671004 | pubmed:author | pubmed-author:UrbainJJ | lld:pubmed |
| pubmed-article:1671004 | pubmed:author | pubmed-author:FUL JLJ | lld:pubmed |
| pubmed-article:1671004 | pubmed:author | pubmed-author:MosesLL | lld:pubmed |
| pubmed-article:1671004 | pubmed:author | pubmed-author:AbramowiczDD | lld:pubmed |
| pubmed-article:1671004 | pubmed:author | pubmed-author:DoutrelepontJ... | lld:pubmed |
| pubmed-article:1671004 | pubmed:author | pubmed-author:VanderhaegenM... | lld:pubmed |
| pubmed-article:1671004 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1671004 | pubmed:volume | 83 | lld:pubmed |
| pubmed-article:1671004 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1671004 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1671004 | pubmed:pagination | 133-6 | lld:pubmed |
| pubmed-article:1671004 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:1671004 | pubmed:meshHeading | pubmed-meshheading:1671004-... | lld:pubmed |
| pubmed-article:1671004 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1671004 | pubmed:articleTitle | Hyper IgE in stimulatory graft-versus-host disease: role of interleukin-4. | lld:pubmed |
| pubmed-article:1671004 | pubmed:affiliation | Department of Nephrology, Hôpital Erasme, Brussels, Belgium. | lld:pubmed |
| pubmed-article:1671004 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1671004 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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