Complement-Opsonized HIV-1 Alters Cross Talk Between Dendritic Cells and Natural Killer (NK) Cells to Inhibit NK Killing and to Upregulate PD-1, CXCR3, and CCR4 on T Cells

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Fältnamn	Indikatorer	Metadata
000		04965naa a2200445 4500
001		oai:DiVA.org:liu-147922
003		SwePub
008		180523s2018 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1479222 URI
024	7	a https://doi.org/10.3389/fimmu.2018.008992 DOI
040		a (SwePub)liu
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Ellegård, Rada,d 1985-u Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten,Region Östergötland, Klinisk genetik4 aut0 (Swepub:liu)radch21
245	1 0	a Complement-Opsonized HIV-1 Alters Cross Talk Between Dendritic Cells and Natural Killer (NK) Cells to Inhibit NK Killing and to Upregulate PD-1, CXCR3, and CCR4 on T Cells
264		c 2018-04-30
264	1	b FRONTIERS MEDIA SA,c 2018
338		a electronic2 rdacarrier
500		a Funding Agencies\|Swedish Research Council; Swedish Physicians against AIDS Research Foundation; VINNMER for Vinnova; Linkoping University Hospital Research Fund; ALF Grants Region Ostergotland; FORSS; CERiA, University of Malaya [UM.C.625/1/HIR/139]
520		a Dendritic cells (DCs), natural killer (NK) cells, and T cells play critical roles during primary HIV-1 exposure at the mucosa, where the viral particles become coated with complement fragments and mucosa-associated antibodies. The microenvironment together with subsequent interactions between these cells and HIV at the mucosal site of infection will determine the quality of immune response that ensues adaptive activation. Here, we investigated how complement and immunoglobulin opsonization influences the responses triggered in DCs and NK cells, how this affects their cross talk, and what T cell phenotypes are induced to expand following the interaction. Our results showed that DCs exposed to complement-opsonized HIV (C-HIV) were less mature and had a poor ability to trigger IFN-driven NK cell activation. In addition, when the DCs were exposed to C-HIV, the cytotolytic potentials of both NK cells and CD8 T cells were markedly suppressed. The expression of PD-1 as well as co-expression of negative immune checkpoints TIM-3 and LAG-3 on PD-1 positive cells were increased on both CD4 as well as CD8 T cells upon interaction with and priming by NK-DC cross talk cultures exposed to C-HIV. In addition, stimulation by NK-DC cross talk cultures exposed to C-HIV led to the upregulation of CD38, CXCR3, and CCR4 on T cells. Together, the immune modulation induced during the presence of complement on viral surfaces is likely to favor HIV establishment, dissemination, and viral pathogenesis.
650	7	a NATURVETENSKAPx Biologix Immunologi0 (SwePub)106052 hsv//swe
650	7	a NATURAL SCIENCESx Biological Sciencesx Immunology0 (SwePub)106052 hsv//eng
653		a dendritic cells; natural killer cells; complement; HIV; cross talk; checkpoint inhibitors; CXCR3; CCR4
700	1	a Khalid, Mohammadu Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten,King Khalid Univ, Saudi Arabia4 aut0 (Swepub:liu)mohkh49
700	1	a Svanberg, Ceciliau Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten4 aut0 (Swepub:liu)cecsv36
700	1	a Holgersson, Hannau Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten4 aut0 (Swepub:liu)n/a
700	1	a Thoren, Ylvau Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten4 aut0 (Swepub:liu)n/a
700	1	a Wittgren, Mirja Karolinau Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten4 aut0 (Swepub:liu)n/a
700	1	a Hinkula, Jormau Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten4 aut0 (Swepub:liu)jorhi40
700	1	a Nyström, Sofiau Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten,Region Östergötland, Klinisk immunologi och transfusionsmedicin4 aut0 (Swepub:liu)sofny82
700	1	a Shankar, Esaki M.u Univ Malaya, Malaysia; Cent Univ Tamil Nadu, India4 aut
700	1	a Larsson, Marieu Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten4 aut0 (Swepub:liu)marla67
710	2	a Linköpings universitetb Avdelningen för mikrobiologi och molekylär medicin4 org
773	0	t Frontiers in Immunologyd : FRONTIERS MEDIA SAg 9q 9x 1664-3224
856	4	u https://liu.diva-portal.org/smash/get/diva2:1209565/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
856	4	u https://www.frontiersin.org/articles/10.3389/fimmu.2018.00899/pdf
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-147922
856	4 8	u https://doi.org/10.3389/fimmu.2018.00899

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