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rdf:type |
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lifeskim:mentions |
umls-concept:C0017349,
umls-concept:C0018133,
umls-concept:C0021853,
umls-concept:C0023693,
umls-concept:C0037083,
umls-concept:C0039194,
umls-concept:C0871261,
umls-concept:C1332714,
umls-concept:C1420817,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1710082,
umls-concept:C2349975,
umls-concept:C2911692
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pubmed:issue |
8
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pubmed:dateCreated |
2005-4-7
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pubmed:abstractText |
Inhibition of LIGHT (a cellular ligand for herpes virus entry mediator and lymphotoxin receptor)/herpes simplex virus entry mediator (HVEM) and LIGHT/lymphotoxin beta receptor (LT beta R) interactions decreases mortality in MHC class I and II disparate graft-vs-host disease (GVHD). The present studies assessed the effects of these interactions on the generation of CD4+ T cell alloresponses in MHC class II-disparate MLC and GVHD. An inhibitor protein of LIGHT and LT alpha beta2 (LT beta R-Ig) and an inhibitor protein of LIGHT (HVEM-Ig) caused similar decreases in alloresponses of control B6 or B6.129S1-IL12rb2(tm1Jm) (B6.IL12R-/-) spleen cells (SpC) in a MHC class II-disparate MLC. GVHD-induced wasting disease in MHC class II-disparate recipients of B6 CD4+ SpC who received either the LT beta R-Ig-encoding adenovirus (LT beta R-Ig Adv; 13.1 +/- 10.9%; n = 10; p = 0.0004) or the HVEM-Ig-encoding adenovirus (HVEM-Ig Adv; 16.4 +/- 9.9%; n = 13; p = 0.0008) was significantly reduced compared with that in recipients of a control adenovirus (30.4 +/- 8.8%; n = 13). Furthermore, gut GVHD histologic scores of recipients of B6 CD4+ SpC who received the LT beta R-Ig Adv (0.8 +/- 0.8; n = 5; p = 0.0007) or the HVEM-Ig Adv (1.4 +/- 0.5; n = 5; p = 0.008) were reduced compared with scores of recipients of a control adenovirus (2.5 +/- 0.75; n = 11). In the intestine, both LT beta R-Ig Adv and HVEM-Ig Adv decreased CD4+ T cells (0.35 +/- 0.4 x 10(6) (n = 6) vs 0.36 +/- 0.02 x 10(6) (n = 9); p = 0.03 and p = 0.007) compared with control adenovirus (0.86 +/- 0.42 x 10(6); n = 9). LIGHT is critical for optimal CD4+ T cell alloresponses in MHC class II-disparate MLC and GVHD.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Recombinant,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Isoantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Virus,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfrsf14 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfsf14 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor Ligand...,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
174
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4688-95
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15814693-Animals,
pubmed-meshheading:15814693-Base Sequence,
pubmed-meshheading:15814693-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15814693-Cell Proliferation,
pubmed-meshheading:15814693-DNA, Recombinant,
pubmed-meshheading:15814693-Female,
pubmed-meshheading:15814693-Graft vs Host Disease,
pubmed-meshheading:15814693-Histocompatibility Antigens Class II,
pubmed-meshheading:15814693-Interferon-gamma,
pubmed-meshheading:15814693-Interleukin-12,
pubmed-meshheading:15814693-Intestines,
pubmed-meshheading:15814693-Isoantigens,
pubmed-meshheading:15814693-Male,
pubmed-meshheading:15814693-Membrane Proteins,
pubmed-meshheading:15814693-Mice,
pubmed-meshheading:15814693-Mice, Inbred C57BL,
pubmed-meshheading:15814693-Mice, Knockout,
pubmed-meshheading:15814693-Mice, Transgenic,
pubmed-meshheading:15814693-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:15814693-Receptors, Tumor Necrosis Factor, Member 14,
pubmed-meshheading:15814693-Receptors, Virus,
pubmed-meshheading:15814693-Recombinant Proteins,
pubmed-meshheading:15814693-Signal Transduction,
pubmed-meshheading:15814693-Tumor Necrosis Factor Ligand Superfamily Member 14,
pubmed-meshheading:15814693-Tumor Necrosis Factor-alpha
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pubmed:year |
2005
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pubmed:articleTitle |
IL-12-independent LIGHT signaling enhances MHC class II disparate CD4+ T cell alloproliferation, IFN-gamma responses, and intestinal graft-versus-host disease.
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pubmed:affiliation |
Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75235-9151, USA. geri.brown@utsouthwestern.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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