Th3 immune responses in the progression of leprosy via molecular cross-talks of TGF-β, CTLA-4 and Cbl-b

Th3 immune responses in the progression of leprosy via molecular cross-talks of TGF-β, CTLA-4 and Cbl-b

Crown Copyright © 2011. Published by Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 141(2011), 2 vom: 05. Nov., Seite 133-42
1. Verfasser: Kumar, Sudhir (VerfasserIn)
Weitere Verfasser: Naqvi, Raza A, Khanna, Neena, Pathak, Pankaj, Rao, D N
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2011
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Comparative Study Journal Article Research Support, Non-U.S. Gov't Adaptor Proteins, Signal Transducing Antibodies, Monoclonal Antigens, Bacterial CTLA-4 Antigen Cytokines RNA, Small Interfering Transforming Growth Factor beta mehr... CBLB protein, human EC 2.3.2.27 Proto-Oncogene Proteins c-cbl
Beschreibung
Zusammenfassung:Crown Copyright © 2011. Published by Elsevier Inc. All rights reserved.
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
Beschreibung:Date Completed 20.12.2011
Date Revised 01.12.2018
published: Print-Electronic
CommentIn: Clin Immunol. 2011 Nov;141(2):127. - PMID 21903479
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2011.06.007