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Abderaouf Damouche Thierry Lazure Véronique Avettand-Fèno?l Nicolas Huot Nathalie Dejucq-Rainsford Anne-Pascale Satie Adeline Mélard Ludivine David Céline Gommet Jade Ghosn Nicolas Noel Guillaume Pourcher Valérie Martinez Stéphane Benoist Véronique Béréziat Antonio Cosma Benoit Favier Bruno Vaslin Christine Rouzioux Jacqueline Capeau Michaela Müller-Trutwin Nathalie Dereuddre-Bosquet Roger Le Grand Olivier Lambotte Christine Bourgeois 《PLoS pathogens》2015,11(9)
Two of the crucial aspects of human immunodeficiency virus (HIV) infection are (i) viral persistence in reservoirs (precluding viral eradication) and (ii) chronic inflammation (directly associated with all-cause morbidities in antiretroviral therapy (ART)-controlled HIV-infected patients). The objective of the present study was to assess the potential involvement of adipose tissue in these two aspects. Adipose tissue is composed of adipocytes and the stromal vascular fraction (SVF); the latter comprises immune cells such as CD4+ T cells and macrophages (both of which are important target cells for HIV). The inflammatory potential of adipose tissue has been extensively described in the context of obesity. During HIV infection, the inflammatory profile of adipose tissue has been revealed by the occurrence of lipodystrophies (primarily related to ART). Data on the impact of HIV on the SVF (especially in individuals not receiving ART) are scarce. We first analyzed the impact of simian immunodeficiency virus (SIV) infection on abdominal subcutaneous and visceral adipose tissues in SIVmac251 infected macaques and found that both adipocytes and adipose tissue immune cells were affected. The adipocyte density was elevated, and adipose tissue immune cells presented enhanced immune activation and/or inflammatory profiles. We detected cell-associated SIV DNA and RNA in the SVF and in sorted CD4+ T cells and macrophages from adipose tissue. We demonstrated that SVF cells (including CD4+ T cells) are infected in ART-controlled HIV-infected patients. Importantly, the production of HIV RNA was detected by in situ hybridization, and after the in vitro reactivation of sorted CD4+ T cells from adipose tissue. We thus identified adipose tissue as a crucial cofactor in both viral persistence and chronic immune activation/inflammation during HIV infection. These observations open up new therapeutic strategies for limiting the size of the viral reservoir and decreasing low-grade chronic inflammation via the modulation of adipose tissue-related pathways. 相似文献
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Phospholipase D Activation Is an Early Component of the Salicylic Acid Signaling Pathway in Arabidopsis Cell Suspensions
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Herfs M Herman L Hubert P Minner F Arafa M Roncarati P Henrotin Y Boniver J Delvenne P 《Cancer immunology, immunotherapy : CII》2009,58(4):603-614
Although human papillomavirus (HPV) DNA is detected in the majority of squamous intraepithelial lesions (SIL) and carcinoma
(SCC) of the uterine cervix, the persistence or progression of cervical lesions suggest that viral antigens are not adequately
presented to the immune system. This hypothesis is reinforced by the observation that most SIL show quantitative and functional
alterations of Langerhans cells (LC). The aim of this study was to determine whether prostaglandins (PG) may affect LC density
in the cervical (pre)neoplastic epithelium. We first demonstrated that the epithelial expression of PGE2 enzymatic pathways, including cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase 1 (mPGES-1), is higher in
SIL and SCC compared to the normal exocervical epithelium and inversely correlated to the density of CD1a-positive LC. By
using cell migration assays, we next showed that the motility of immature dendritic cells (DC) and DC partially differentiated
in vitro in the presence of PGE2 are differentially affected by PGE2. Immature DC had a lower ability to migrate in the presence of PGE2 compared to DC generated in vitro in the presence of PGE2. Finally, we showed that PGE2 induced a cytokine production profile and phenotypical features of tolerogenic DC, suggesting that the altered expression
of PGE2 enzymatic pathways may promote the cervical carcinogenesis by favouring (pre)cancer immunotolerance.
M. Herfs and L. Herman contributed equally to this work. 相似文献
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Prakash SK LeMaire SA Guo DC Russell L Regalado ES Golabbakhsh H Johnson RJ Safi HJ Estrera AL Coselli JS Bray MS Leal SM Milewicz DM Belmont JW 《American journal of human genetics》2010,87(6):743-756
Thoracic aortic aneurysms and dissections (TAAD) cause significant morbidity and mortality, but the genetic origins of TAAD remain largely unknown. In a genome-wide analysis of 418 sporadic TAAD cases, we identified 47 copy number variant (CNV) regions that were enriched in or unique to TAAD patients compared to population controls. Gene ontology, expression profiling, and network analysis showed that genes within TAAD CNVs regulate smooth muscle cell adhesion or contractility and interact with the smooth muscle-specific isoforms of α-actin and β-myosin, which are known to cause familial TAAD when altered. Enrichment of these gene functions in rare CNVs was replicated in independent cohorts with sporadic TAAD (STAAD, n = 387) and inherited TAAD (FTAAD, n = 88). The overall prevalence of rare CNVs (23%) was significantly increased in FTAAD compared with STAAD patients (Fisher's exact test, p = 0.03). Our findings suggest that rare CNVs disrupting smooth muscle adhesion or contraction contribute to both sporadic and familial disease. 相似文献
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Maaran Michael Rajah Mathieu Hubert Elodie Bishop Nell Saunders Remy Robinot Ludivine Grzelak Delphine Planas Jrmy Dufloo Stacy Gellenoncourt Alice Bongers Marija Zivaljic Cyril Planchais Florence GuivelBenhassine Franoise Porrot Hugo Mouquet Lisa A Chakrabarti Julian Buchrieser Olivier Schwartz 《The EMBO journal》2021,40(24)
Severe COVID‐19 is characterized by lung abnormalities, including the presence of syncytial pneumocytes. Syncytia form when SARS‐CoV‐2 spike protein expressed on the surface of infected cells interacts with the ACE2 receptor on neighboring cells. The syncytia forming potential of spike variant proteins remain poorly characterized. Here, we first assessed Alpha (B.1.1.7) and Beta (B.1.351) spread and fusion in cell cultures, compared with the ancestral D614G strain. Alpha and Beta replicated similarly to D614G strain in Vero, Caco‐2, Calu‐3, and primary airway cells. However, Alpha and Beta formed larger and more numerous syncytia. Variant spike proteins displayed higher ACE2 affinity compared with D614G. Alpha, Beta, and D614G fusion was similarly inhibited by interferon‐induced transmembrane proteins (IFITMs). Individual mutations present in Alpha and Beta spikes modified fusogenicity, binding to ACE2 or recognition by monoclonal antibodies. We further show that Delta spike also triggers faster fusion relative to D614G. Thus, SARS‐CoV‐2 emerging variants display enhanced syncytia formation. 相似文献
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Aynur Snmez Rasem Mustafa Salome T. Ryll Francesca Tuorto Ludivine Wacheul Donatella Ponti Christian Litke Tanja Hering Kerstin Kojer Jenniver Koch Claudia Pitzer Joachim Kirsch Andreas Neueder Grzegorz Kreiner Denis L. J. Lafontaine Michael Orth Birgit Liss Rosanna Parlato 《Cell death & disease》2021,12(12)