| A cytokine inducible SH2-domain protein (CISH), significantly induced during DC development, plays an important role in DC-mediated CTL activation. | |
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MedLine Citation:
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PMID: 22002016 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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The cytokine inducible SH2-domain protein (CISH) is a well known STAT5 target gene, but its role in the immune system remains uncertain. In this study, we found that CISH is predominantly induced during dendritic cell (DC) development from mouse bone marrow (BM) cells, and plays a crucial role in type 1 DC development and DC-mediated CTL activation. CISH-knockdown reduced the expression of MHC class I, co-stimulatory molecules and pro-inflammatory cytokines in BMDCs. Meanwhile, the DC yield was markedly enhanced by CISH-knockdown via cell cycle activation and reduction of cell apoptosis. Down-regulation of cell proliferation at the later stage of DC development was found to be associated with CISH-mediated negative feedback regulation of STAT-5 activation. In T-cell immunity, OT-1 T-cell proliferation was significantly reduced by CISH-knockdown in DCs while OT-2 T-cell proliferation was not affected by CISH-knockdown. CTLs generated by DC vaccination were also markedly reduced by CISH-knockdown, followed by significant impairment of DC-based tumor immunotherapy. Taken together, our data suggest that CISH expression at the later stage of DC development triggers the shutdown of DC progenitor cell proliferation, and facilitates DC differentiation into a potent stimulator of CTLs. |
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Authors:
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Mohammad Alam Miah; Cheol-Hee Yoon; Joonoh Kim; Jinah Jang; Young-Rim Seong; Yong-Soo Bae |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-10-17 |
Journal Detail:
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Title: European journal of immunology Volume: - ISSN: 1521-4141 ISO Abbreviation: - Publication Date: 2011 Oct |
Date Detail:
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Created Date: 2011-10-17 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 1273201 Medline TA: Eur J Immunol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. |
Affiliation:
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Department of Biological Sciences, Sungkyunkwan University, Suwon, Gyeonggi-do 440-746, South Korea. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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