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Deciphering the Acylation Pattern of Yersinia enterocolitica Lipid A

Deciphering the Acylation Pattern of Yersinia enterocolitica Lipid A | Host Cell & Pathogen Interactions | Scoop.it
Pathogenic bacteria may modify their surface to evade the host innate immune response. Yersinia enterocolitica modulates its lipopolysaccharide (LPS) lipid A structure, and the key regulatory signal is temperature. At 21°C, lipid A is hexa-acylated and may be modified with aminoarabinose or palmitate. At 37°C, Y. enterocolitica expresses a tetra-acylated lipid A consistent with the 3′-O-deacylation of the molecule.
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Host Cell & Pathogen Interactions
Strategies of Microbial Virulence and Host Defense
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Antiviral immunity Dual attack by RIG-I - Nature.com

Antiviral immunity Dual attack by RIG-I
Nature.com
A recent study in Immunity describes a novel antiviral role for the cytosolic sensor RIG-I. Sato et al.

Via Gilbert Faure au nom de l'ASSIM
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Gilbert Faure au nom de l'ASSIM's curator insight, January 19, 2:13 PM

A recent study in Immunity describes a novel antiviral role for the cytosolic sensor RIG-I. Sato et al. show that RIG-I not only induces an interferon (IFN) response during hepatitis B virus (HBV) infection, but also directly suppresses viral replication by blocking the binding of the HBV polymerase to the pre-genomic RNA (pgRNA) of the virus…

 http://www.scoop.it/t/immunology?q=rig

 

from WIKIPEDIA

RIG-I (retinoic acid-inducible gene 1) is a RIG-I-like receptor dsRNA helicase enzyme that is encoded (in humans) by the DDX58 gene. RIG-I is part of the RIG-I-like receptor family, which also includes MDA5 and LGP2, and functions as a pattern recognition receptor that is a sensor for viruses such as influenza A, Sendai virus, and flavivirus, however RIG-I provides no immunity to DNA viruses or retroviruses. RIG-I typically recognizes short (< 4000nt) 5′ triphosphate uncapped double stranded or single stranded RNA.[1][2][3] RIG-I and MDA5 are involved in activating MAVS and triggering an antiviral response.[4] RIG-I is also able to detect non-self 5′-triphosphorylated dsRNA transcribed from AT-rich dsDNA by DNA-dependent RNA polymerase III (Pol III). For many viruses, effective RIG-I-mediated antiviral responses are dependent on functionally active LGP2.[5]

 







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IFITM3 Restricts Influenza A Virus Entry by Blocking the Formation of Fusion Pores following Virus-Endosome Hemifusion

IFITM3 Restricts Influenza A Virus Entry by Blocking the Formation of Fusion Pores following Virus-Endosome Hemifusion | Host Cell & Pathogen Interactions | Scoop.it
From molecules to physiology
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Review of evidence for immune evasion and persistent infection in Lyme disease

@MGKatz036 @skepticpedi http://t.co/KyDatJCNQA "we can conclude chronic LD patients suffer from symptoms related to persistent infection"

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Gilbert Faure au nom de l'ASSIM's curator insight, January 3, 3:00 PM

This review describes known and suspected mechanisms by which spirochetes of the Borrelia genus evade host immune defenses and survive antibiotic challenge. Accumulating evidence indicates that Lyme disease spirochetes are adapted to persist in immune competent hosts, and that they are able to remain infective despite aggressive antibiotic challenge. Advancing understanding of the survival mechanisms of the Lyme disease spirochete carry noteworthy implications for ongoing research and clinical practice.

2013

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Access : Kr|[uuml]|ppel-like factor 4 negatively regulates cellular antiviral immune response : Cellular & Molecular Immunology

Cellular and Molecular Immunology aims to report the dynamic progress being made in China and abroad in immunological research, and welcomes high-quality Research Articles, Reviews and Brief Reports across a broad range of topics including, but not limited to, clinical immunology, comparative immunology, immunobiology, immunogenetics, immunological techniques, immunopathology, immunopharmacology, infection immunology, neuroimmunology, transplantation immunology, tumor immunology, and veterinary immunology.

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Gilbert Faure au nom de l'ASSIM's curator insight, January 7, 5:14 AM

Viral infection triggers activation of the transcription factors NF-κB and IRF3, which collaborate to induce the expression of type I interferons (IFNs) and elicit innate antiviral response. In this report, we identified Krüppel-like factor 4 (KLF4) as a negative regulator of virus-triggered signaling. Overexpression of KLF4 inhibited virus-induced activation of ISRE and IFN-β promoter in various types of cells, while knockdown of KLF4 potentiated viral infection-triggered induction of IFNB1 and downstream genes and attenuated viral replication. In addition, KLF4 was found to be localized in the cytosol and nucleus, and viral infection promoted the translocation of KLF4 from cytosol to nucleus. Upon virus infection, KLF4 was bound to the promoter of IFNB gene and inhibited the recruitment of IRF3 to the IFNB promoter. Our study thus suggests that KLF4 negatively regulates cellular antiviral response.

 
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The Immunoreceptor TIGIT Regulates Antitumor and Antiviral CD8+ T Cell Effector Function: Cancer Cell

The Immunoreceptor TIGIT Regulates Antitumor and Antiviral CD8+ T Cell Effector Function: Cancer Cell | Host Cell & Pathogen Interactions | Scoop.it
RT @genentech: New paper from our scientists in @Cancer_Cell shows how TIGIT may be potential #immunotherapy target http://t.co/FswC0GF9YB

 

Highlights

 

•Human and murine tumor-infiltrating CD8+ T cells express high levels of TIGIT•Antibody coblockade of TIGIT and PDL1 elicits tumor rejection in preclinical models•TIGIT selectively limits the effector function of chronically stimulated CD8+T cells•TIGIT interacts with CD226 in cis and disrupts CD226 homodimerization

 

Summary

Tumors constitute highly suppressive microenvironments in which infiltrating T cells are “exhausted” by inhibitory receptors such as PD-1. Here we identify TIGIT as a coinhibitory receptor that critically limits antitumor and other CD8+ T cell-dependent chronic immune responses. TIGIT is highly expressed on human and murine tumor-infiltrating T cells, and, in models of both cancer and chronic viral infection, antibody coblockade of TIGIT and PD-L1 synergistically and specifically enhanced CD8+ T cell effector function, resulting in significant tumor and viral clearance, respectively. This effect was abrogated by blockade of TIGIT’s complementary costimulatory receptor, CD226, whose dimerization is disrupted upon direct interaction with TIGIT in cis. These results define a key role for TIGIT in inhibiting chronic CD8+ T cell-dependent responses.


Via Krishan Maggon , Gilbert Faure au nom de l'ASSIM
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Krishan Maggon 's curator insight, December 13, 2014 1:32 AM

Cancer Cell

 

The Immunoreceptor TIGIT Regulates Antitumor and Antiviral CD8+ T Cell Effector FunctionRobert J. Johnston, Laetitia Comps-Agrar, Jason Hackney, Xin Yu, Mahrukh Huseni, Yagai Yang, Summer Park, Vincent Javinal, Henry Chiu, Bryan Irving,Dan L. Eaton, Jane L. Grogan DOI: http://dx.doi.org/10.1016/j.ccell.2014.10.018
Gilbert Faure au nom de l'ASSIM's curator insight, December 13, 2014 2:28 AM

TIGIT?

http://en.wikipedia.org/wiki/TIGIT

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Human Viruses and Cancer

Human Viruses and Cancer | Host Cell & Pathogen Interactions | Scoop.it
To date, seven viruses have been consistently linked to different types of human cancer, and infections are estimated to account for up to 20% of all cancer cases worldwide.

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pH-Dependent entry of chikungunya virus fusion into mosquito cells

Millions of human infections caused by arthropod-borne pathogens are initiated by the feeding of an infected mosquito on a vertebrate. However, interactions between the viruses and the mosquito vector, which facilitates successful infection and transmission of virus to a subsequent vertebrate host, are still not fully understood.
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E5564 inhibits immunosuppressive cytokine IL-10 induction promoted by HIV-1 Tat protein

In HIV-1 infected patients, production of interleukin-10 (IL-10), a highly immunosuppressive cytokine, is associated with progression of infection toward AIDS. HIV-1 Tat protein, by interacting with TLR4-MD2 at the membrane level, induces IL-10 production by primary human monocytes and macrophages. In the present study we evaluated the effect of the TLR4 antagonist Eritoran tetrasodium (E5564) on HIV-1 Tat-induced IL-10 production.
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Immune Checkpoint Inhibitors for Renal Cell Carcinoma - Targeted Oncology

Immune Checkpoint Inhibitors for Renal Cell Carcinoma - Targeted Oncology | Host Cell & Pathogen Interactions | Scoop.it
It is estimated that 1 in 63 individuals in the United States will develop renal cell carcinoma (RCC), making it among the most common cancers in the country.

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Gilbert Faure au nom de l'ASSIM's curator insight, November 27, 2014 1:28 PM

Binding of PD-1 to B7-H1 and B7-DC inhibits signaling via phosphatidylinositol-3 kinase and its downstream target, AKT. This inhibition leads to downstream events responsible for decreased T-cell proliferation and survival. It also decreases protein synthesis in T cells and cytokine production.3 Therapies based on monoclonal antibodies directed against PD1 and its ligands (immune checkpoint blockade) are emerging as novel therapeutic options for patients with various solid tumors as well as hematologic malignancies, including RCC. Checkpoint inhibitors in RCC will be the subject of this review. - See more at: http://www.targetedonc.com/publications/targeted-therapies-cancer/2014/october-2014/Immune-Checkpoint-Inhibitors-for-Renal-Cell-Carcinoma#sthash.BlDdXafS.dpuf

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Small Things Considered: Why CRISPR Doesn't Work in E. coli

Small Things Considered: Why CRISPR Doesn't Work in E. coli | Host Cell & Pathogen Interactions | Scoop.it
by Elio | We received this query: »I enjoyed the article on your blog 'Six Questions About CRISPRs' by Merry Youle. I am an ex-lambdologist, having quit phage lambda in the early 70s and moved to GM-plants. There is one thing about CRISPR that I do not understand: Why did lambdologists not find CRISPR?
They found phage...
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Atypical MHC class II-expressing antigen-presenting cells: can anything replace a dendritic cell?

Atypical MHC class II-expressing antigen-presenting cells: can anything replace a dendritic cell? | Host Cell & Pathogen Interactions | Scoop.it

Dendritic cells, macrophages and B cells are regarded as the classical antigen-presenting cells of the immune system. However, in recent years, there has been a rapid increase in the number of cell types that are suggested to present antigens on MHC class II molecules to CD4+ T cells. In this Review, we describe the key characteristics that define an antigen-presenting cell by examining the functions of dendritic cells. We then examine the functions of the haematopoietic cells and non-haematopoietic cells that can express MHC class II molecules and that have been suggested to represent 'atypical' antigen-presenting cells. We consider whether any of these cell populations can prime naive CD4+ T cells and, if not, question the effects that they do have on the development of immune responses.


Via Krishan Maggon , Gilbert Faure au nom de l'ASSIM
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Krishan Maggon 's curator insight, November 15, 2014 9:22 AM
Atypical MHC class II-expressing antigen-presenting cells: can anything replace a dendritic cell?Taku Kambayashi& Terri M. LauferAffiliationsCorresponding authorNature Reviews Immunology 14, 719–730 (2014) doi:10.1038/nri3754Published online 17 October 2014
Gilbert Faure au nom de l'ASSIM's curator insight, November 16, 2014 1:09 PM

and epithelial cells in autoimmunity

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Host-Specific Parvovirus Evolution in Nature Is Recapitulated by In Vitro Adaptation to Different Carnivore Species

Host-Specific Parvovirus Evolution in Nature Is Recapitulated by In Vitro Adaptation to Different Carnivore Species | Host Cell & Pathogen Interactions | Scoop.it
From molecules to physiology
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Influenza A virus uses the aggresome processing machinery for host cell entry

During cell entry, capsids of incoming influenza A viruses (IAVs) must be uncoated before viral ribonucleoproteins (vRNPs) can enter the nucleus for replication. After hemagglutinin-mediated membrane fusion in late endocytic vacuoles, the vRNPs and the matrix proteins dissociate from each other and disperse within the cytosol. Here, we found that for capsid disassembly, IAV takes advantage of the host cell’s aggresome formation and disassembly machinery. The capsids mimicked misfolded protein aggregates by carrying unanchored ubiquitin chains that activated a histone deacetylase 6 (HDAC6)–dependent pathway. The ubiquitin-binding domain was essential for recruitment of HDAC6 to viral fusion sites and for efficient uncoating and infection. That other components of the aggresome processing machinery, including dynein, dynactin, and myosin II, were also required suggested that physical forces generated by microtubule- and actin-associated motors are essential for IAV entry.


Via burkesquires, Mel Melendrez-Vallard
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SOCS3 and STAT3, major controllers of the outcome of infection with... - PubMed - NCBI

Semin Immunol. 2014 Nov 1;26(6):518-532. doi: 10.1016/j.smim.2014.10.004. [Epub ahead of print] REVIEW

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The RNA Sensor RIG-I Dually Functions as an Innate Sensor and Direct Antiviral Factor for Hepatitis B Virus: Immunity

The RNA Sensor RIG-I Dually Functions as an Innate Sensor and Direct Antiviral Factor for Hepatitis B Virus: Immunity | Host Cell & Pathogen Interactions | Scoop.it
The RNA Sensor RIG-I Dually Functions as an Innate Sensor and Direct Antiviral Factor for Hepatitis B Virus #inmuva http://t.co/SxZlYehxVs

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The E3 Ubiquitin Ligase AMFR and INSIG1 Bridge the Activation of TBK1 Kinase by Modifying the Adaptor STING: Immunity

The E3 Ubiquitin Ligase AMFR and INSIG1 Bridge the Activation of TBK1 Kinase by Modifying the Adaptor STING: Immunity | Host Cell & Pathogen Interactions | Scoop.it
Wang lab show how activated STING recruits TBK1 for innate immune signaling http://t.co/KVGlu0RXuc

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Gilbert Faure au nom de l'ASSIM's curator insight, January 7, 5:13 AM

STING in focus

•STING signaling is drastically abolished in Amfr−/− cells•AMFR catalyzes K27-linked polyubiquitination of STING, which depends on INSIG1•The K27-linked polyubiquitin on STING facilitates TBK1 recruitment and activation•Myeloid-cell-specific Insig1−/− mice are more susceptible to HSV-1 infection
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Crosstalk between Edc4 and Mammalian Target of Rapamycin Complex 1 (mTORC1) Signaling in mRNA Decapping

Crosstalk between Edc4 and Mammalian Target of Rapamycin Complex 1 (mTORC1) Signaling in mRNA Decapping | Host Cell & Pathogen Interactions | Scoop.it
The mammalian target of rapamycin complex 1 (mTORC1) is involved in the cellular transcription and translation processes. The undertaken study characterized the enhancer of mRNA decapping protein 4 (Edc4) as mTORC1 interacting protein. Human T lymphoblast (CCRF-CEM) cells were used for mTORC1 purification. Co-immunoprecipitation coupled with immunoblotting analysis was used to confirm the interaction of Edc4 in mTORC1 specific purifications. Further assays were incorporated to conclude the role of mTORC1 in mRNA decapping via Edc4. Edc4 was identified as a new interacting protein with mTORC1 in both the endogenous and myc-tag raptor component mTORC1 specific purifications. Quantitative co-localization using confocal microscopy demonstrated that raptor component of mTORC1 coexists with Edc4 in processing (P) bodies, a site for mRNA degradation. Incubation of cells with rapamycin, a known inhibitor of mTOR kinase activity, increased the total Edc4 protein expression but at the same time decreased the Edc4 interaction with mTORC1. Moreover, rapamycin treatment resulted in a significant decrease in total serine phosphorylated Edc4 protein signal and the total 5'-capped mRNA. These findings provide the first evidence for the pivotal role of mTORC1 in Edc4 regulation. Further in-depth studies are required to get a complete understanding of molecular crosstalk between mTORC1 signaling and mRNA decapping pathway.
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An Evolutionary Battle Against Bacteria

An Evolutionary Battle Against Bacteria | Host Cell & Pathogen Interactions | Scoop.it
A recent study illustrates how our ancestors evolved new defenses to starve meningitis-causing bacteria of the iron they need to grow.
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Functions of Heat Shock Proteins in Pathways of the Innate and Adaptive Immune System [BRIEF REVIEWS]

For more than 50 years, heat shock proteins (HSPs) have been studied for their role in protecting cells from elevated temperature and other forms of stress. More recently, several roles have been ascribed to HSPs in the immune system.

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Gilbert Faure au nom de l'ASSIM's curator insight, December 12, 2014 4:13 AM
Abstract

For more than 50 years, heat shock proteins (HSPs) have been studied for their role in protecting cells from elevated temperature and other forms of stress. More recently, several roles have been ascribed to HSPs in the immune system. These include intracellular roles in Ag presentation and expression of innate receptors, as well as extracellular roles in tumor immunosurveillance and autoimmunity. Exogenously administered HSPs can elicit a variety of immune responses that have been used in immunotherapy of cancer, infectious diseases, and autoimmune disease.

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MicroRNA miR-320a and miR-140 inhibit mink enteritis virus infection by repression of its receptor, feline transferrin receptor

Mink enteritis virus (MEV) is one of the most important pathogens in the mink industry. Recent studies have shed light into the role of microRNAs (miRNAs), small noncoding RNAs of length ranging from 18¿23 nucleotides (nt), as critical modulators in the host-pathogen interaction networks. We previously showed that miRNA miR-181b can inhibit MEV replication by repression of viral non-structural protein 1 expression. Here, we report that two other miRNAs (miR-320a and miR-140) inhibit MEV entry into feline kidney (F81) cells by downregulating its receptor, transferrin receptor (TfR), by targeting the 3¿ untranslated region (UTR) of TfR mRNA, while being themselves upregulated.
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Building viruses that kill cancer cells: BeneVir gets $2M, waiting on $10M more

Building viruses that kill cancer cells: BeneVir gets $2M, waiting on $10M more | Host Cell & Pathogen Interactions | Scoop.it
Maryland startup BeneVir is developing immunotherapy viruses that rid the body of two types of tumor cells - those that cause cancer and the ones that make it recurrent.

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How ZMapp antibodies bind to Ebola virus

How ZMapp antibodies bind to Ebola virus | Host Cell & Pathogen Interactions | Scoop.it
The structure of the antibodies in ZMapp bound to the Ebola virus glycoprotein reveal how they inhibit infection and how ZMapp might be improved.
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Scripps Research Institute Scientists Reveal Weak Spots in Ebola’s Defenses

Scripps Research Institute Scientists Reveal Weak Spots in Ebola’s Defenses | Host Cell & Pathogen Interactions | Scoop.it
News Release
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What Makes Ebola So Deadly? [VIDEO]

What Makes Ebola So Deadly? [VIDEO] | Host Cell & Pathogen Interactions | Scoop.it
The Ebola virus is able to kill its victim so quickly because of its effective warfare against a body's immune system.
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Alfonso Barrios Sanz's curator insight, November 11, 2014 7:29 AM

The strain currently affecting is the most severe. This strain produces a strong hemorrhagic fever. Also it is a very contagious virus, so we have to take high security methods. 

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Coronavirus Cell Entry Occurs through the Endo-/Lysosomal Pathway in a Proteolysis-Dependent Manner

Coronavirus Cell Entry Occurs through the Endo-/Lysosomal Pathway in a Proteolysis-Dependent Manner | Host Cell & Pathogen Interactions | Scoop.it
From molecules to physiology
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