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排序方式: 共有118条查询结果,搜索用时 171 毫秒
81.
Translocation products in acute myeloid leukemia activate the Wnt signaling pathway in hematopoietic cells 总被引:13,自引:0,他引:13
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82.
Ozensoy O Nishimori I Vullo D Puccetti L Scozzafava A Supuran CT 《Bioorganic & medicinal chemistry》2005,13(22):6089-6093
The first inhibition study of the transmembrane carbonic anhydrase (CA, EC 4.2.1.1) isozymes hCA XIV with a library of aromatic and heteroaromatic sulfonamides synthesized earlier is reported. Most of the inhibitors were sulfanilamide, homosulfanilamide and 4-aminoethyl-benzenesulfonamide derivatives, to which tails that would induce diverse physicochemical properties have been attached at the amino moiety. Several of these compounds were metanilamide, benzene-1,3-disulfonamide or the 1,3,4-thiadiazole/thiadiazoline-2-sulfonamide derivatives. The tails incorporated in these molecules were of the alkyl/aryl-carboxamido/ sulfonamido-, ureido- or thioureido-types. The sulfanilamides acylated at the 4-amino group with short aliphatic/aromatic moieties incorporating 2-6 carbon atoms showed modest hCA XIV inhibitory activity (K(I)-s in the range of 1.25-4.2 microM) which were anyhow better than that of sulfanilamide (K(I) of 5.4 microM). Better activity showed the homosulfanilamide and 4-aminoethyl-benzenesulfonamide derivatives bearing arylsulfonamido/ureido and thioureido moieties, with K(I)'s in the range of 203-935 nM. The best activity was observed for the heteroaromatic compounds incorporating 1,3,4-thiadiazole/thiadiazoline-2-sulfonamide and 5-arylcarboxamido/sulfonamido moieties, with K(I)'s in the range of 10-85 nM. All these compounds were generally also much better inhibitors of the other two transmembrane CA isozyme, hCA IX and XII. Thus, highly potent hCA XIV inhibitors were detected, but isozyme-specific inhibitors were not discovered for the moment. 相似文献
83.
SE?Aleshin AV?Timofeev MV?Khoretonenko LG?Zakharova GV?Pashvykina JR?Stephenson AM?Shneider AD?AltsteinEmail author 《BMC microbiology》2005,5(1):45
Background
Heterologous prime-boost immunization protocols using different gene expression systems have proven to be successful tools in protecting against various diseases in experimental animal models. The main reason for using this approach is to exploit the ability of expression cassettes to prime or boost the immune system in different ways during vaccination procedures. The purpose of the project was to study the ability of recombinant vaccinia virus (VV) and bacterial plasmid, both carrying the NS1 gene from tick-borne encephalitis (TBE) virus under the control of different promoters, to protect mice against lethal challenge using a heterologous prime-boost vaccination protocol. 相似文献84.
T cell apoptosis by tryptophan catabolism 总被引:20,自引:0,他引:20
Fallarino F Grohmann U Vacca C Bianchi R Orabona C Spreca A Fioretti MC Puccetti P 《Cell death and differentiation》2002,9(10):1069-1077
Indoleamine 2,3-dioxygenase (IDO) is a tryptophan-catabolizing enzyme that, expressed by different cell types, has regulatory effects on T cells resulting from tryptophan depletion in specific local tissue microenvironments. Different mechanisms, however, might contribute to IDO-dependent immune regulation. We show here that tryptophan metabolites in the kynurenine pathway, such as 3-hydroxyanthranilic and quinolinic acids, will induce the selective apoptosis in vitro of murine thymocytes and of Th1 but not Th2 cells. T cell apoptosis was observed at relatively low concentrations of kynurenines, did not require Fas/Fas ligand interactions, and was associated with the activation of caspase-8 and the release of cytochrome c from mitochondria. When administered in vivo, the two kynurenines caused depletion of specific thymocyte subsets in a fashion qualitatively similar to dexamethasone. These data suggest that the selective deletion of T lymphocytes may be a major mechanism whereby tryptophan metabolism affects immunity under physiopathologic conditions. 相似文献
85.
86.
87.
Gibson S Kibiki Bert Mulder Wil MV Dolmans Jessica L de Beer Martin Boeree Noel Sam Dick van Soolingen Christophe Sola Adri GM van der Zanden 《BMC microbiology》2007,7(1):51
Background
Tuberculosis (TB) is a major health problem and HIV is the major cause of the increase in TB. Sub-Saharan Africa is endemic for both TB and HIV infection. Determination of the prevalence of M. tuberculosis strains and their drug susceptibility is important for TB control. 相似文献88.
Ursula Grohmann Maria Laura Belladonna Roberta Bianchi Ciriana Orabona Silvia Silla Giuseppe Squillacioti Maria Cristina Fioretti Paolo Puccetti 《Cancer immunology, immunotherapy : CII》1999,48(4):195-203
Nonameric P815AB, a cytotoxic-T-lymphocyte-defined minimal core peptide encoded by the murine mastocytoma gene P1A, fails to initiate CD4+ cell-dependent reactivity in vivo to class-I-restricted epitopes when mice are administered peptide-pulsed dendritic cells.
Effective immunization requires T helper effects, such as those mediated by coimmunization with class-II-restricted (helper)
peptides or by the use of recombinant interleukin-12 (rIL-12). Although P815AB does possess class-II-restricted epitopes,
they are likely suboptimal, resulting in poor affinity and/or stability of MHC/P815AB complexes and inadequate activation
of the antigen-presenting cell function of dendritic cells. The present study has examined a series of longer, P815AB-centered
peptides (11–14 amino acids in length, all P1A-encoded) for their ability to initiate CD4+ and CD8+ cell-mediated responses to the nonamer in vivo, their ability to bind class II MHC in vitro, and their ability to assemble
class II molecules stably. By means of a class-I-restricted skin test assay in mice receiving peptide-pulsed dendritic cells,
we found that a 12-mer and a 13-mer effectively immunized against the core P815AB peptide, and that this correlated with IL-2
production in vitro by CD4+ cells in response to the nonamer. In vitro studies, involving affinity-purified class II molecules, showed that the capacity
to assemble class II molecules stably, more than the affinity for class II MHC, correlated with the ability of the different
P815AB peptides to prime the host to the core peptide seen by the T cells.
Received: 25 February 1999 / Accepted: 14 April 1999 相似文献
89.
Distinct roles of immunoreceptor tyrosine‐based motifs in immunosuppressive indoleamine 2,3‐dioxygenase 1
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Marco Gargaro Giada Mondanelli Maria L. Belladonna Maria Teresa Pallotta Claudia Volpi Francesca Fallarino Antonio Macchiarulo Cinzia Antognelli Roberta Bianchi Carmine Vacca Paolo Puccetti Ursula Grohmann Ciriana Orabona 《Journal of cellular and molecular medicine》2017,21(1):165-176
The enzyme indoleamine 2,3‐dioxygenase 1 (IDO1) catalyses the initial, rate‐limiting step in tryptophan (Trp) degradation, resulting in tryptophan starvation and the production of immunoregulatory kynurenines. IDO1's catalytic function has long been considered as the one mechanism responsible for IDO1‐dependent immune suppression by dendritic cells (DCs), which are master regulators of the balance between immunity and tolerance. However, IDO1 also harbours immunoreceptor tyrosine‐based inhibitory motifs, (ITIM1 and ITIM2), that, once phosphorylated, bind protein tyrosine phosphatases, (SHP‐1 and SHP‐2), and thus trigger an immunoregulatory signalling in DCs. This mechanism leads to sustained IDO1 expression, in a feedforward loop, which is particularly important in restraining autoimmunity and chronic inflammation. Yet, under specific conditions requiring that early and protective inflammation be unrelieved, tyrosine‐phosphorylated ITIMs will instead bind the suppressor of cytokine signalling 3 (SOCS3), which drives IDO1 proteasomal degradation and shortens the enzyme half‐life. To dissect any differential roles of the two IDO1's ITIMs, we generated protein mutants by replacing one or both ITIM‐associated tyrosines with phospho‐mimicking glutamic acid residues. Although all mutants lost their enzymic activity, the ITIM1 – but not ITIM2 mutant – did bind SHPs and conferred immunosuppressive effects on DCs, making cells capable of restraining an antigen‐specific response in vivo. Conversely, the ITIM2 mutant would preferentially bind SOCS3, and IDO1's degradation was accelerated. Thus, it is the selective phosphorylation of either ITIM that controls the duration of IDO1 expression and function, in that it dictates whether enhanced tolerogenic signalling or shutdown of IDO1‐dependent events will occur in a local microenvironment. 相似文献
90.
Elisa Tinazzi Marzia Dolcino Antonio Puccetti Antonella Rigo Ruggero Beri Maria Teresa Valenti Roberto Corrocher Claudio Lunardi 《Arthritis research & therapy》2010,12(4):R131-15