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231224s2011 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2011.06.007
|2 doi
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|a pubmed24n0701.xml
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|a (DE-627)NLM210424095
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|a (NLM)21807564
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
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|a Kumar, Sudhir
|e verfasserin
|4 aut
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|a Th3 immune responses in the progression of leprosy via molecular cross-talks of TGF-β, CTLA-4 and Cbl-b
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|c 2011
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 20.12.2011
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|a Date Revised 01.12.2018
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|a published: Print-Electronic
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|a CommentIn: Clin Immunol. 2011 Nov;141(2):127. - PMID 21903479
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|a Citation Status MEDLINE
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| 520 |
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|a Crown Copyright © 2011. Published by Elsevier Inc. All rights reserved.
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|a Leprosy is a chronic human disease; primarily affecting skin, peripheral nerves, eyes, testis etc. Comprehensive-expressional-profiling of Th1-Th2-Th3 associated markers (84 genes) using qRT-PCR array, negated the previously prevailing notion, Th2 bias towards multibacillary stage of leprosy. High production TGF-β further supported the dearth of any immune response(s) in leprosy progression. Over expression of Cbl-b, could emerge as plausible reason for contributing T cell hyporesponsiveness, possibly by degradation of T cells signaling molecules. Anti-TGF-β treatments further confirm the TGF-β-dependent-Cbl-b overexpression in multibacillary patients. Diminished Cbl-b expression in CTLA-4 knockout studies using siRNA, provided other evidence towards T cell hyporesponsiveness. Further, high T cell proliferation and IL-2 production in PBMC cultures treated with anti-TGF-β and siRNA offers here a strategy to revert T cell hyporesponsiveness by downregulating Cbl-b expression in leprosy. Thus, this study negates Th2 bias and substantiates molecular cross-talk amongst TGF-β-CTLA-4-Cbl-b eventually leads to M. leprae persistence
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|a Comparative Study
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Adaptor Proteins, Signal Transducing
|2 NLM
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| 650 |
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|a Antibodies, Monoclonal
|2 NLM
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| 650 |
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|a Antigens, Bacterial
|2 NLM
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| 650 |
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|a CTLA-4 Antigen
|2 NLM
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| 650 |
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|a Cytokines
|2 NLM
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| 650 |
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|a RNA, Small Interfering
|2 NLM
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| 650 |
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|a Transforming Growth Factor beta
|2 NLM
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| 650 |
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|a CBLB protein, human
|2 NLM
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| 650 |
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|a EC 2.3.2.27
|2 NLM
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| 650 |
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|a Proto-Oncogene Proteins c-cbl
|2 NLM
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| 650 |
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|a EC 2.3.2.27
|2 NLM
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| 700 |
1 |
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|a Naqvi, Raza A
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Khanna, Neena
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Pathak, Pankaj
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Rao, D N
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 141(2011), 2 vom: 05. Nov., Seite 133-42
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
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|g volume:141
|g year:2011
|g number:2
|g day:05
|g month:11
|g pages:133-42
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|u http://dx.doi.org/10.1016/j.clim.2011.06.007
|3 Volltext
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