Immunology
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Rescooped by Gilbert C FAURE from Curation & The Future of Publishing
onto Immunology
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30 years of Content Curation summarized in 1 tweet?


Via Guillaume Decugis
Gilbert C FAURE's insight:

from current contents and reprint requests to now!

eugene garfield, what do you think of changes of scientific virtual networking?

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Larry's comment, May 9, 2013 5:47 AM
But the three 83, 93, 03 are delivered directly ... to see it with scoopit, you have to subscribe to the sender scoop... and which one when he has several ? Function to be added : generating an email for direct notification ...
Guillaume Decugis's comment, May 9, 2013 11:30 AM
@Larry: isn't that what our "create a newsletters" function does? To see it go to one of your topics and click on Manage.
Emmanuel 'Manny' Gigante's curator insight, May 9, 2013 3:39 PM

6this just says it alll

Immunology
Teaching and Learning Immunology. Information you never would have searched for!
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The TOP 10% information you need!

The topics gathering around 20K highly selected scoops over 40 months, compared to 200K  or 400K results found with Pubmed or Google Scholar respectively. The scoops deal with published (classical or OPEN) and grey literature (blogs, websites, social networks, press releases) allowing rapid access to recently published relevant information

 

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Gilbert C FAURE's insight:

This topic is focusing mainly on fundamental systemic immunology.

 

Feel free to browse other related topics!

Mucosal Immunity:

 http://www.scoop.it/t/mucosal-immunity

Immunology and Biotherapies

http://www.scoop.it/t/immunology-and-biotherapies

Autoimmunity

http://www.scoop.it/t/autoimmunity

Allergy and clinical immunology:

http://www.scoop.it/t/allergy-and-clinical-immunology

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History of Immunology

http://www.scoop.it/t/history-of-immunology

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Gilbert C FAURE's curator insight, July 15, 2016 12:55 PM
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Software maps immune system in 17 days (not 106 years)

Software maps immune system in 17 days (not 106 years) | Immunology | Scoop.it
A team of scientists has created a genetic map of all possible receptors the human immune system might generate—also known as the immunome. The proje
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Corpse Engulfment Generates a Molecular Memory that Primes the Macrophage Inflammatory Response. - PubMed - NCBI

Cell. 2016 Jun 16;165(7):1658-71. doi: 10.1016/j.cell.2016.04.049. Epub 2016 May 19. Research Support, Non-U.S. Gov't
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Abstract Macrophages are multifunctional cells that perform diverse roles in health and disease. Emerging evidence has suggested that these innate immune cells might also be capable of developing immunological memory, a trait previously associated with the adaptive system alone. While recent studies have focused on the dramatic macrophage reprogramming that follows infection and protects against secondary microbial attack, can macrophages also develop memory in response to other cues? Here, we show that apoptotic corpse engulfment by Drosophila macrophages is an essential primer for their inflammatory response to tissue damage and infection in vivo. Priming is triggered via calcium-induced JNK signaling, which leads to upregulation of the damage receptor Draper, thus providing a molecular memory that allows the cell to rapidly respond to subsequent injury or infection. This remarkable plasticity and capacity for memory places macrophages as key therapeutic targets for treatment of inflammatory disorders.
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Common Variable Immune Deficiency | Immune Deficiency Foundation

Common Variable Immune Deficiency | Immune Deficiency Foundation | Immunology | Scoop.it
If you want to learn more about my condition please watch House Season 1 episode 17: Role Model until you get it.... https://t.co/kt7SFR9GdR
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Vasculitides and the Complement System: a Comprehensive Review. - PubMed - NCBI

Vasculitides and the Complement System: a Comprehensive Review. - PubMed - NCBI | Immunology | Scoop.it
Clin Rev Allergy Immunol. 2015 Dec;49(3):333-46. doi: 10.1007/s12016-014-8453-8. Review
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T memory stem cells in health and disease : Nature Medicine : Nature Research

T memory stem cells in health and disease : Nature Medicine : Nature Research | Immunology | Scoop.it
Gattinoni and colleagues discuss the emerging roles of this subset of long-lived memory T lymphocytes, and highlight ways in which these cells might be exploited to achieve therapeutic aims.
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Innate and adaptive immune traits are differentially affected by genetic and environmental factors

Innate and adaptive immune traits are differentially affected by genetic and environmental factors | Immunology | Scoop.it
Both genetics and environment affect the number and phenotype of immune cells. Here the authors characterize the degree of influence of genetics versus environment on various immune cell parameters by analysing a large cohort of female twins.
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the paper previously commented
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Combined immunodeficiency and Epstein-Barr virus–induced B cell malignancy in humans with inherited CD70 deficiency

Combined immunodeficiency and Epstein-Barr virus–induced B cell malignancy in humans with inherited CD70 deficiency | Immunology | Scoop.it
In this study, we describe four patients from two unrelated families of different ethnicities with a primary immunodeficiency, predominantly manifesting as susceptibility to Epstein-Barr virus (EBV)–related diseases. Three patients presented with EBV-associated Hodgkin’s lymphoma and hypogammaglobulinemia; one also had severe varicella infection. The fourth had viral encephalitis during infancy. Homozygous frameshift or in-frame deletions in CD70 in these patients abolished either CD70 surface expression or binding to its cognate receptor CD27. Blood lymphocyte numbers were normal, but the proportions of memory B cells and EBV-specific effector memory CD8+ T cells were reduced. Furthermore, although T cell proliferation was normal, in vitro–generated EBV-specific cytotoxic T cell activity was reduced because of CD70 deficiency. This reflected impaired activation by, rather than effects during killing of, EBV-transformed B cells. Notably, expression of 2B4 and NKG2D, receptors implicated in controlling EBV infection, on memory CD8+ T cells from CD70-deficient individuals was reduced, consistent with their impaired killing of EBV-infected cells. Thus, autosomal recessive CD70 deficiency is a novel cause of combined immunodeficiency and EBV-associated diseases, reminiscent of inherited CD27 deficiency. Overall, human CD70–CD27 interactions therefore play a nonredundant role in T and B cell–mediated immunity, especially for protection against EBV and humoral immunity.
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TCR Signaling and CD28/CTLA-4 Signaling Cooperatively Modulate T Regulatory Cell Homeostasis

TCR Signaling and CD28/CTLA-4 Signaling Cooperatively Modulate T Regulatory Cell Homeostasis Michael P. Holt*, George A. Punkosdy†,‡, Deborah D. Glass* and Ethan M. Shevach* *Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda,...
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Revisiting the regulatory roles of the TGF-β family of cytokines. - PubMed - NCBI

Revisiting the regulatory roles of the TGF-β family of cytokines. - PubMed - NCBI | Immunology | Scoop.it
Autoimmun Rev. 2016 Sep;15(9):917-22. doi: 10.1016/j.autrev.2016.07.007. Epub 2016 Jul 5. Review
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Frontiers | Editorial: HSPs—Ambiguous Mediators of Immunity | Vaccines and Molecular Therapeutics

Frontiers | Editorial: HSPs—Ambiguous Mediators of Immunity | Vaccines and Molecular Therapeutics | Immunology | Scoop.it
Editorial: HSPs—Ambiguous Mediators of Immunity
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JCI Insight - Interlesional diversity of T cell receptors in melanoma with immune checkpoints enriched in tissue-resident memory T cells

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Frontiers | Retinoic Acid Signaling in B Cells Is Required for the Generation of an Effective T-Independent Immune Response | B Cell Biology

Frontiers | Retinoic Acid Signaling in B Cells Is Required for the Generation of an Effective T-Independent Immune Response | B Cell Biology | Immunology | Scoop.it
Retinoic acid (RA) plays an important role in the balance of inflammation and tolerance in T cells. Furthermore, it has been demonstrated that RA facilitates IgA isotype switching in B cells in vivo. However, it is unclear whether RA has a direct effect on T-independent B cell responses in vivo. To address this question, we generated a mouse model where RA signalling in the B cell lineage is specifically silenced. This was achieved through the overexpression of a dominant negative receptor for RA (dnRAR) in the B cell lineage. In this model, we found a dramatic reduction in marginal zone B cells and accumulation of transitional 2 B cells in the spleen. We also observed a reduction in B1 B cells in the peritoneum with a defect in the T-independent B cell response against 2,4,6-trinitrophenyl (TNP). This was not a result of inhibited development of B cells in the bone marrow but likely the result of both, defective expression of S1P1 in MZ B cells and a defect in the development of MZ and B1 B cells. This suggests that RAR expression in B cells is important for the B cell frequency in the marginal zone and peritoneum to generate an efficient T-independent humoral response.
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Rescooped by Gilbert C FAURE from Immunology, vaccine & infectious diseases
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Class II MHC-independent suppressive adhesion of dendritic cells by regulatory T cells in vivo. - PubMed - NCBI

Class II MHC-independent suppressive adhesion of dendritic cells by regulatory T cells in vivo. - PubMed - NCBI | Immunology | Scoop.it
J Exp Med. 2017 Jan 12. pii: jem.20160629. doi: 10.1084/jem.20160629. [Epub ahead of print]

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Denis Hudrisier's curator insight, January 17, 1:00 PM
This paper and another one in JEM show that Treg stick to DC to prevent access and priming of cognate T cells
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Lipin-2 regulates NLRP3 inflammasome by affecting P2X7 receptor activation

Lipin-2 regulates NLRP3 inflammasome by affecting P2X7 receptor activation | Immunology | Scoop.it
Mutations in human LPIN2 produce a disease known as Majeed syndrome, the clinical manifestations of which are ameliorated by strategies that block IL-1β or its receptor. However the role of lipin-2 during IL-1β production remains elusive. We show here that lipin-2 controls excessive IL-1β formation in primary human and mouse macrophages by several mechanisms, including activation of the inflammasome NLRP3. Lipin-2 regulates MAPK activation, which mediates synthesis of pro–IL-1β during inflammasome priming. Lipin-2 also inhibits the activation and sensitization of the purinergic receptor P2X7 and K+ efflux, apoptosis-associated speck-like protein with a CARD domain oligomerization, and caspase-1 processing, key events during inflammasome activation. Reduced levels of lipin-2 in macrophages lead to a decrease in cellular cholesterol levels. In fact, restoration of cholesterol concentrations in cells lacking lipin-2 decreases ion currents through the P2X7 receptor, and downstream events that drive IL-1β production. Furthermore, lipin-2–deficient mice exhibit increased sensitivity to high lipopolysaccharide doses. Collectively, our results unveil lipin-2 as a critical player in the negative regulation of NLRP3 inflammasome.
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C-type lectin receptor DCIR modulates immunity to tuberculosis by sustaining type I interferon signaling in dendritic cells

C-type lectin receptor DCIR modulates immunity to tuberculosis by sustaining type I interferon signaling in dendritic cells | Immunology | Scoop.it
National Academy of Sciences
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The aryl hydrocarbon receptor controls cell-fate decisions in B cells

The aryl hydrocarbon receptor controls cell-fate decisions in B cells | Immunology | Scoop.it
Generation of cellular heterogeneity is an essential feature of the adaptive immune system. This is best exemplified during humoral immune response when an expanding B cell clone assumes multiple cell fates, including class-switched B cells, antibody-secreting plasma cells, and memory B cells. Although each cell type is essential for immunity, their generation must be exquisitely controlled because a class-switched B cell cannot revert back to the parent isotype, and a terminally differentiated plasma cell cannot contribute to the memory pool. In this study, we show that an environmental sensor, the aryl hydrocarbon receptor (AhR) is highly induced upon B cell activation and serves a critical role in regulating activation-induced cell fate outcomes. We find that AhR negatively regulates class-switch recombination ex vivo by altering activation-induced cytidine deaminase expression. We further demonstrate that AhR suppresses class switching in vivo after influenza virus infection and immunization with model antigens. In addition, by regulating Blimp-1 expression via Bach2, AhR represses differentiation of B cells into plasmablasts ex vivo and antibody-secreting plasma cells in vivo. These experiments suggest that AhR serves as a molecular rheostat in B cells to brake the effector response, possibly to facilitate optimal recall responses. Thus, AhR might represent a novel molecular target for manipulation of B cell responses during vaccination.
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Scientists Discover New Subtype of Immune Cell

A recent study from the Immunology Frontier Research Center (IFReC) in Japan led to the discovery of a new group of monocytes with a strange morphology tha
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The newly discovered lymphocytes were described as having a “bi-lobed segmented nuclear shape and many cytoplasmic granules by IFReC professor Shizuo Akira. He and his team thus called the new cells “segregated nucleus atypical monocytes,” or “SatM.” Observations from Akira’s team led to the realization that these new cells could be responsible for causing fibrosis, scarring that can be dangerous if unattended due to a thickening of the tissues, in mice.
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The histone demethylase UTX regulates the lineage-specific epigenetic program of invariant natural killer T cells

Invariant natural killer T cells (iNKT cells) are innate-like lymphocytes that protect against infection, autoimmune disease and cancer. However, little is known about the epigenetic regulation of iNKT cell development. Here we found that the H3K27me3 histone demethylase UTX was an essential cell-intrinsic factor that controlled an iNKT-cell lineage-specific gene-expression program and epigenetic landscape in a demethylase-activity-dependent manner. UTX-deficient iNKT cells exhibited impaired expression of iNKT cell signature genes due to a decrease in activation-associated H3K4me3 marks and an increase in repressive H3K27me3 marks within the promoters occupied by UTX. We found that JunB regulated iNKT cell development and that the expression of genes that were targets of both JunB and the iNKT cell master transcription factor PLZF was UTX dependent. We identified iNKT cell super-enhancers and demonstrated that UTX-mediated regulation of super-enhancer accessibility was a key mechanism for commitment to the iNKT cell lineage. Our findings reveal how UTX regulates the development of iNKT cells through multiple epigenetic mechanisms.
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Mature IgM-expressing plasma cells sense antigen and develop competence for cytokine production upon antigenic challenge

Mature IgM-expressing plasma cells sense antigen and develop competence for cytokine production upon antigenic challenge | Immunology | Scoop.it
Plasma cells produce secreted antibodies and are thought to lack expression of the membrane-bound immunoglobulins that constitute B-cell receptors.
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ICC Birmingham boosts system with ESID 2020 Immunodeficiencies Congress

ICC Birmingham boosts system with ESID 2020 Immunodeficiencies Congress | Immunology | Scoop.it
Birmingham’s International Convention Centre (ICC) has secured the European Society for Immunodeficiencies (ESID) Congress in 2020. The venue and the city won the bid over competing cities Brussels and Geneva.

The congress, which brings together the
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Disease tolerance and immunity in host protection against infection : Nature Reviews Immunology : Nature Research

Disease tolerance and immunity in host protection against infection : Nature Reviews Immunology : Nature Research | Immunology | Scoop.it
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Inhibition of RORγT Skews TCRα Gene Rearrangement and Limits T Cell Repertoire Diversity

Inhibition of RORγT Skews TCRα Gene Rearrangement and Limits T Cell Repertoire Diversity | Immunology | Scoop.it
Guo et al. find that small-molecule RORγT antagonist treatment induces CD4+CD8+ thymocyte
apoptosis, skews the T cell repertoire, prevents autoreactive T cell development,
and delays autoimmune EAE progression. This work underscores the risk versus benefit
of targeting RORγT in clinical testing of RORγT inhibitors.
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Generation of a Novel HLA Class I Transgenic Mouse Model Carrying a Knock-in Mutation at the β2-Microglobulin Locus

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The human thymus perivascular space is a functional niche for viral-specific plasma cells

The human thymus perivascular space is a functional niche for viral-specific plasma cells | Immunology | Scoop.it
The human thymus is the seat of T cell production, and thymic infection can alter both thymopoiesis and tolerance. Circulating antibodies from bone marrow–resident plasma cells have been shown to help protect the thymus from infection; however, the contribution of thymic-resident B cells has remained unclear. Now, Nuñez et al . report that plasma cells reside in the human thymus and that these plasma cells produce antibodies reactive to common viral proteins. These cells inhabit the thymic perivascular space, located between the thymic epithelial areas and the circulation, and therefore may fortify the thymus against pathogen invasion. These cells are maintained in aging individuals, suggesting that thymic plasma cells play a key role in thymic protection throughout the human life span.
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