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rdf:type |
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lifeskim:mentions |
umls-concept:C0011209,
umls-concept:C0021368,
umls-concept:C0033684,
umls-concept:C0111208,
umls-concept:C0205314,
umls-concept:C0442118,
umls-concept:C0679622,
umls-concept:C0700624,
umls-concept:C1160185,
umls-concept:C1292733,
umls-concept:C1511625,
umls-concept:C1514562,
umls-concept:C1880389,
umls-concept:C1883204,
umls-concept:C1883221
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pubmed:issue |
5
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pubmed:dateCreated |
2006-5-5
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pubmed:abstractText |
CTLA-4 is a negative regulator of T-cell activation, and its inhibitory effects can be accomplished either by competition with CD28 or by transmitting negative signals through its intracellular domain. To utilize the cytoplasmic domain of CTLA-4 to suppress allergic inflammation, we fused it to a novel protein-transduction domain in the human transcriptional factor Hph-1. Transduction efficiency was verified in vitro and in vivo after ocular, intranasal and intradermal administration. After transduction into T cells, the Hph-1-ctCTLA-4 fusion protein inhibited the production of interleukin (IL)-2, and downregulated CD69 and CD25. Intranasal administration of Hph-1-ctCTLA-4 resulted in markedly reduced infiltration of inflammatory cells, secretion of T helper type 2 (T(H)2) cytokines, serum IgE levels and airway hyper-responsiveness in a mouse model of allergic airway inflammation. These results indicated that Hph-1-ctCTLA-4 constitutes an effective immunosuppressive protein drug for potential use in the treatment of allergic asthma, via nasal administration.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA-4 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ctla4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoconjugates,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin,
http://linkedlifedata.com/resource/pubmed/chemical/PHC1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1078-8956
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pubmed:author |
pubmed-author:AhnMi-HyunMH,
pubmed-author:ChaeWook-JinWJ,
pubmed-author:ChoiJe-MinJM,
pubmed-author:JungYung-GookYG,
pubmed-author:KimEun-SungES,
pubmed-author:KimKyun-DoKD,
pubmed-author:KimYoung-EunYE,
pubmed-author:LeeDong-HoDH,
pubmed-author:LeeJung-HoonJH,
pubmed-author:LeeSang-KyouSK,
pubmed-author:LeeSeung-KyouSK,
pubmed-author:ParkChoon-SikCS,
pubmed-author:ParkJae-ChulJC,
pubmed-author:ParkJung-WonJW,
pubmed-author:ParkTae-KwannTK,
pubmed-author:SeoByung-FhyBF,
pubmed-author:ShinJung-AhJA,
pubmed-author:SongHyun-MiHM
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pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
574-9
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:16604087-Administration, Intranasal,
pubmed-meshheading:16604087-Animals,
pubmed-meshheading:16604087-Antigens, CD,
pubmed-meshheading:16604087-Antigens, Differentiation,
pubmed-meshheading:16604087-Asthma,
pubmed-meshheading:16604087-Bronchial Hyperreactivity,
pubmed-meshheading:16604087-CTLA-4 Antigen,
pubmed-meshheading:16604087-Carrier Proteins,
pubmed-meshheading:16604087-Female,
pubmed-meshheading:16604087-Humans,
pubmed-meshheading:16604087-Immunoconjugates,
pubmed-meshheading:16604087-Immunosuppressive Agents,
pubmed-meshheading:16604087-Inflammation,
pubmed-meshheading:16604087-Male,
pubmed-meshheading:16604087-Mice,
pubmed-meshheading:16604087-Mice, Inbred BALB C,
pubmed-meshheading:16604087-Ovalbumin,
pubmed-meshheading:16604087-Protein Structure, Tertiary,
pubmed-meshheading:16604087-Recombinant Fusion Proteins,
pubmed-meshheading:16604087-Transduction, Genetic
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pubmed:year |
2006
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pubmed:articleTitle |
Intranasal delivery of the cytoplasmic domain of CTLA-4 using a novel protein transduction domain prevents allergic inflammation.
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pubmed:affiliation |
Department of Biotechnology, College of Engineering, Yonsei University, Seoul 120-749, Republic of Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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