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  • 1
    Online Resource
    Online Resource
    Zinc signals promote IL‐2‐dependent proliferation of T cells
    Wiley ; 2010
    In:  European Journal of Immunology Vol. 40, No. 5 ( 2010-05), p. 1496-1503
    Details
    In: European Journal of Immunology, Wiley, Vol. 40, No. 5 ( 2010-05), p. 1496-1503
    Abstract: Zinc signals, i.e. a change of the intracellular concentration of free zinc ions in response to receptor stimulation, are involved in signal transduction in several immune cells. Here, the role of zinc signals in T‐cell activation by IL‐2 was investigated in the murine cytotoxic T‐cell line CTLL‐2 and in primary human T cells. Measurements with the fluorescent dyes FluoZin‐3 and Zinquin showed that zinc is released from lysosomes into the cytosol in response to stimulation of the IL‐2‐receptor. Activation of the ERK‐pathway was blocked by chelation of free zinc with N , N , N ′, N ′‐tetrakis‐2(pyridyl‐methyl)ethylenediamine, whereas zinc was not required for STAT5 phosphorylation. In addition, the key signaling molecules MEK and ERK were activated in response to elevated free intracellular zinc, induced by incubation with zinc and the ionophore pyrithione. Downstream of ERK activation, ERK‐specific gene expression of c‐fos and IL‐2‐induced proliferation was found to depend on zinc. Further experiments indicated that inhibition of MEK and ERK‐dephosphorylating protein phosphatases is the molecular mechanism for the influence of zinc on this pathway. In conclusion, an increase of cytoplasmic free zinc is required for IL‐2‐induced ERK signaling and proliferation of T cells.
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    URL: Article
    DOI: 10.1002/eji.v40:5
    DOI: 10.1002/eji.200939574
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2010
    detail.hit.zdb_id: 1491907-2
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  • 2
    Online Resource
    Online Resource
    Differential Regulation of TLR-Dependent MyD88 and TRIF Signaling Pathways by Free Zinc Ions
    The American Association of Immunologists ; 2013
    In:  The Journal of Immunology Vol. 191, No. 4 ( 2013-08-15), p. 1808-1817
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 191, No. 4 ( 2013-08-15), p. 1808-1817
    Abstract: Zinc signals are utilized by several immune cell receptors. One is TLR4, which causes an increase of free zinc ions (Zn2+) that is required for the MyD88-dependent expression of inflammatory cytokines. This study investigates the role of Zn2+ on Toll/IL-1R domain–containing adapter inducing IFN-β (TRIF)–dependent signals, the other major intracellular pathway activated by TLR4. Chelation of Zn2+ with the membrane-permeable chelator N,N,N’,N’-Tetrakis(2-pyridylmethyl)ethylenediamine augmented TLR4-mediated production of IFN-β and subsequent synthesis of inducible NO synthase and production of NO. The effect is based on Zn2+ acting as a negative regulator of the TRIF pathway via reducing IFN regulatory factor 3 activation. This was also observed with TLR3, the only TLR that signals exclusively via TRIF, but not MyD88, and does not trigger a zinc signal. In contrast, IFN-γ–induced NO production was unaffected by N,N,N’,N’-Tetrakis(2-pyridylmethyl)ethylenediamine. Taken together, Zn2+ is specifically involved in TLR signaling, where it differentially regulates MyD88 and TRIF signaling via a zinc signal or via basal Zn2+ levels, respectively.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1301261
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2013
    detail.hit.zdb_id: 1475085-5
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  • 3
    Online Resource
    Online Resource
    Cellular zinc homeostasis is a regulator in monocyte differentiation of HL-60 cells by 1α,25-dihydroxyvitamin D3
    Oxford University Press (OUP) ; 2010
    In:  Journal of Leukocyte Biology Vol. 87, No. 5 ( 2010-01-20), p. 833-844
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 87, No. 5 ( 2010-01-20), p. 833-844
    Abstract: A decrease of free cellular zinc promotes monocyte differentiation of HL-60 cells by alleviating zinc-mediated inhibition of adenylate cyclase. It was reported previously that zinc-deficient mice show impaired lymphopoiesis. At the same time, monocyte numbers in these animals are increased, indicating a negative impact of zinc on monocyte development. Here, we investigate the role of zinc homeostasis in the differentiation of myeloid precursors into monocytes. Reduced gene expression of several zinc transporters, predominantly from the Zip family, was observed during 1α, 25-dihydroxyvitamin D3 (1,25D3)-induced differentiation of HL-60 cells. This was accompanied by a reduction of intracellular-free zinc, measured by FluoZin-3. Amplifying this reduction with the zinc chelator TPEN or zinc-depleted cell-culture medium enhanced 1,25D3-induced expression of monocytic surface markers CD11b and CD14 on HL-60, THP-1, and NB4 cells. In contrast, differentiation of NB4 cells to granulocytes was not zinc-sensitive, pointing toward a specific effect of zinc on monocyte differentiation. Further, monocyte functions, such as TNF-α secretion, phagocytosis, and oxidative burst, were also augmented by differentiation in the presence of TPEN. The second messenger cAMP promotes monocyte differentiation. We could show that zinc inhibits the cAMP-synthesizing enzyme adenylate cyclase, and chelation of zinc by TPEN increases cAMP generation after stimulation with the adenylate cyclase activator forskolin. Based on our in vitro results and the in vivo observations from the literature, we suggest a model in which the intracellular-free zinc concentration limits AC activity, and the decrease of zinc after 1,25D3 treatment promotes differentiation by relieving AC inhibition. Thus, cellular zinc homeostasis acts as an endogenous modulator of monocyte differentiation.
    Type of Medium: Online Resource
    ISSN: 1938-3673 , 0741-5400
    URL: Article
    DOI: 10.1189/jlb.0409241
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2010
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Susceptibility to tuberculosis is associated with TLR1 polymorphisms resulting in a lack of TLR1 cell surface expression
    Oxford University Press (OUP) ; 2011
    In:  Journal of Leukocyte Biology Vol. 90, No. 2 ( 2011-06-03), p. 377-388
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 90, No. 2 ( 2011-06-03), p. 377-388
    Abstract: Human TLR1 plays an important role in host defense against Mycobacterium tuberculosis. Our aim was to analyze the association of the loss of TLR1 surface expression and TLR1 SNPs with susceptibility to TB. TLR1neg and TLR1pos cells from healthy individuals were identified by flow cytometry and compared by sequencing. TLR1 expression was measured using quantitative real-time PCR and immunoblotting. TLR1 SNP analyses of healthy individuals and TB patients from EU-C and Ghana were performed, and association of the TLR1 genotypes with increased risk of developing TB was statistically evaluated. Lack of TLR1 surface expression accompanied by impaired function was strongly associated with TLR1 SNP G743A. Genotyping of EU-C controls and TB patients revealed an association of TLR1 743A/1805G alleles [OR 2.37 (95% CI 1.13, 4.93), P=0.0219; OR 2.74 (95% CI 1.26, 6.05), P=0.0059] as well as TLR1neg 743AA/1805GG versus TLR1pos genotypes 743AG/1805TG [OR 4.98 (95% CI 1.64, 15.15), P=0.0034; OR 5.70 (95% CI 1.69, 20.35), P=0.0015] and 743AG + GG/1805TG + TT [OR 3.54 (95% CI 1.29, 9.90), P=0.0086; OR 4.17 (95% CI 1.52, 11.67), P=0.0025] with increased susceptibility to TB. No association of G743A with TB was found in Ghana as a result of a low frequency of genotype 743AA. Our data gain new insights in the role of TLR1 in M. tuberculosis defense and provide the first evidence that TLR1 variants are associated with susceptibility to TB in a low-incidence country.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    URL: Article
    DOI: 10.1189/jlb.0409233
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2011
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    An Element of Life: Competition for Zinc in Host-Pathogen Interaction
    Elsevier BV ; 2013
    In:  Immunity Vol. 39, No. 4 ( 2013-10), p. 623-624
    Details
    In: Immunity, Elsevier BV, Vol. 39, No. 4 ( 2013-10), p. 623-624
    Type of Medium: Online Resource
    ISSN: 1074-7613
    URL: Article
    DOI: 10.1016/j.immuni.2013.09.009
    RVK:
    XA 48754.8
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2013
    detail.hit.zdb_id: 2001966-X
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