Cholera toxin, and the related nontoxic adjuvants mmCT and dmLT, promote human Th17 responses via cyclic AMP-protein kinase A and inflammasome-dependent IL-1 signaling

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Fältnamn	Indikatorer	Metadata
000		05287naa a2200601 4500
001		oai:gup.ub.gu.se/221525
003		SwePub
008		240910s2015 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://gup.ub.gu.se/publication/2215252 URI
024	7	a https://doi.org/10.4049/jimmunol.14016332 DOI
040		a (SwePub)gu
041		a eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Larena, Maximilianu Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi,Institute of Biomedicine, Department of Microbiology and Immunology4 aut0 (Swepub:gu)xlarma
245	1 0	a Cholera toxin, and the related nontoxic adjuvants mmCT and dmLT, promote human Th17 responses via cyclic AMP-protein kinase A and inflammasome-dependent IL-1 signaling
264		c 2015-04-15
264	1	b The American Association of Immunologists,c 2015
520		a We have examined the molecular pathways involved in the adjuvant action of cholera toxin (CT) and two novel nontoxic molecules, multiple-mutated CT (mmCT) and double-mutant heat-labile toxin (dmLT) on human T cell responses. Human PBMCs or isolated monocytes were stimulated in vitro with CT, mmCT, or dmLT plus a polyclonal stimulus (staphylococcal enterotoxin B) or specific bacterial Ags, and effects on expression of cytokines and signaling molecules were determined. CT, mmCT, and dmLT strongly enhanced IL-17A and to a lesser extent IL-13 responses, but had little effect on IFN-gamma production or cell proliferation. Intracellular cytokine staining revealed that the enhanced IL-17A production was largely confined to CD4(+) T cells and coculture experiments showed that the IL-17A promotion was effectively induced by adjuvant-treated monocytes. Relative to CT, mmCT and dmLT induced at least 100-fold lower levels of cAMP, yet this cAMP was enough and essential for the promotion of Th17 responses. Thus, inhibition of cAMP-dependent protein kinase A was abolished, and stimulation with a cAMP analog mimicked the adjuvant effect. Furthermore, CT, mmCT, and dmLT induced IL-1beta production and caspase-1 activation in monocytes, which was associated with increased expression of key proinflammatory and inflammasome-related genes, including NLRP1, NLRP3, and NLRC4. Inflammasome inhibition with a specific caspase-1 inhibitor, or blocking of IL-1 signaling by IL-1 receptor antagonist, abrogated the Th17-promoting effect. We conclude that CT, mmCT, and dmLT promote human Th17 responses via cAMP-dependent protein kinase A and caspase-1/inflammasome-dependent IL-1 signaling.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Immunologi inom det medicinska området0 (SwePub)301102 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Immunology in the medical area0 (SwePub)301102 hsv//eng
653		a Adaptor Proteins
653		a Signal Transducing/immunology
653		a Adjuvants
653		a Immunologic/ pharmacology
653		a Adult
653		a Apoptosis Regulatory Proteins/immunology
653		a CARD Signaling Adaptor Proteins/immunology
653		a Calcium-Binding Proteins/immunology
653		a Carrier Proteins/immunology
653		a Caspase 1/immunology
653		a Cholera Toxin/ pharmacology
653		a Cyclic AMP/ immunology
653		a Cyclic AMP-Dependent Protein Kinases/ immunology
653		a Enzyme Activation/drug effects/immunology
653		a Female
653		a Humans
653		a Inflammasomes/ immunology
653		a Interleukin-1beta/ immunology
653		a Male
653		a Middle Aged
653		a Signal Transduction/ drug effects/immunology
653		a Th17 Cells/cytology/ immunology
700	1	a Holmgren, Jan,d 1944u Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi,Institute of Biomedicine, Department of Microbiology and Immunology4 aut0 (Swepub:gu)xholja
700	1	a Lebens, Michael,d 1956u Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi,Institute of Biomedicine, Department of Microbiology and Immunology4 aut0 (Swepub:gu)xlebmi
700	1	a Terrinoni, Manuelau Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi,Institute of Biomedicine, Department of Microbiology and Immunology4 aut0 (Swepub:gu)xterma
700	1	a Lundgren, Anna,d 1974u Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi,Institute of Biomedicine, Department of Microbiology and Immunology4 aut0 (Swepub:gu)xlannj
710	2	a Göteborgs universitetb Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi4 org
773	0	t Journal of Immunologyd : The American Association of Immunologistsg 194:8, s. 3829-39q 194:8<3829-39x 0022-1767x 1550-6606
856	4	u https://www.jimmunol.org/content/jimmunol/194/8/3829.full.pdf
856	4 8	u https://gup.ub.gu.se/publication/221525
856	4 8	u https://doi.org/10.4049/jimmunol.1401633

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