3,371 results match your criteria Current Opinion in Immunology[Journal]


Editorial overview: Pillars of innate immunity: constantly learning and trying to remember.

Curr Opin Immunol 2019 Feb;56:iii-vi

Innate Immunity Unit, Institut Pasteur, Inserm U1223, Paris, France.

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http://dx.doi.org/10.1016/j.coi.2019.03.002DOI Listing
February 2019

Innate sensors that regulate vaccine responses.

Curr Opin Immunol 2019 Apr 9;59:31-41. Epub 2019 Apr 9.

Department of Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. Electronic address:

Pattern recognition receptors (PRRs) control elemental functions of antigen presenting cells (APCs) and critically shape adaptive immune responses. Wielding a natural adjuvanticity, live attenuated vaccines elicit exceptionally efficient and durable immunity. Commonly used vaccine adjuvants target individual PRRs or bolster the immunogenicity of vaccines via indirect mechanisms of inflammation. Read More

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http://dx.doi.org/10.1016/j.coi.2019.02.006DOI Listing

Understanding the immunology of the Zostavax shingles vaccine.

Curr Opin Immunol 2019 Apr 7;59:25-30. Epub 2019 Apr 7.

Emory Vaccine Center and Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA.

Zostavax is a live-attenuated varicella zoster virus (VZV) vaccine recommended for use in adults >50 years of age to prevent shingles. The main risk factor for the development of shingles is age, which correlates with decreasing cell-mediated immunity. These data suggest a predominant role of T cell immunity in controlling VZV latency. Read More

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http://dx.doi.org/10.1016/j.coi.2019.02.005DOI Listing
April 2019
1 Read

Vaccination against atherosclerosis.

Curr Opin Immunol 2019 Mar 28;59:15-24. Epub 2019 Mar 28.

Division of Inflammation Biology, La Jolla Institute for Immunology, La Jolla, CA, United States; Department of Bioengineering, University of California San Diego, La Jolla, CA, United States. Electronic address:

Atherosclerosis is a chronic inflammatory disease that causes most heart attacks and strokes, making it the biggest killer in the world. Although cholesterol-lowering drugs have dramatically reduced these major adverse cardiovascular events, there remains a high residual risk called inflammatory risk. Atherosclerosis has an autoimmune component that can be manipulated by immunologic approaches including vaccination. Read More

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http://dx.doi.org/10.1016/j.coi.2019.02.008DOI Listing
March 2019
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Tfh cell response in influenza vaccines in humans: what is visible and what is invisible.

Authors:
Hideki Ueno

Curr Opin Immunol 2019 Mar 25;59:9-14. Epub 2019 Mar 25.

Department of Microbiology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, Box: 1124, Annenberg Building, Room: 15-14A New York, NY 10029, United States; Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, Box: 1124, Annenberg Building, Room: 15-14A New York, NY 10029, United States. Electronic address:

Elucidating the immune mechanism by which seasonal influenza vaccines induce a protective immune response is of great importance to gain insights into the design of next-generation vaccines conferring more effective and long-lasting immune protection. Recent studies have established that T follicular helper (Tfh) cells play a major role for the generation of antibody response following influenza vaccination. Yet, the evidence is gained largely through the analysis of blood samples, and our knowledge on the role of Tfh cells in influenza vaccination is still largely limited to the generation of antigen-specific plasmablasts. Read More

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http://dx.doi.org/10.1016/j.coi.2019.02.007DOI Listing

Mitochondrial antigen presentation: a mechanism linking Parkinson's disease to autoimmunity.

Curr Opin Immunol 2019 Mar 21;58:31-37. Epub 2019 Mar 21.

Département de Neurosciences, Université de Montréal, CRCHUM, 900 rue Saint-Denis, Montréal, H2X 0A9, Canada. Electronic address:

Parkinson's disease (PD) is caused by the progressive loss of dopaminergic neurons and afflicts millions of people world-wide. The current treatments address only the late motor symptoms, with no cure or preventive therapeutic approaches. The contribution of dysfunctional immune mechanisms in PD has been clearly established, with an emphasis on neuroinflammation and microglial cell activation. Read More

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http://dx.doi.org/10.1016/j.coi.2019.02.004DOI Listing

Studying interactions between dendritic cells and T cells in vivo.

Curr Opin Immunol 2019 Mar 15;58:24-30. Epub 2019 Mar 15.

Laboratory of Lymphocyte Dynamics, The Rockefeller University, New York, NY, USA. Electronic address:

Antigen presentation is the key first step in the establishment of an antigen-specific T cell response. Among professional antigen presenting cells (APCs), dendritic cells (DCs) are the major population responsible for the priming of both CD4 and CD8 naïve T cells. This priming requires physical interaction between the DC and the T cell; during which signals are exchanged that determine both the magnitude and the quality of the ensuing response. Read More

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http://dx.doi.org/10.1016/j.coi.2019.02.002DOI Listing
March 2019
2 Reads

Antigenic cross-reactivity between Zika and dengue viruses: is it time to develop a universal vaccine?

Curr Opin Immunol 2019 Mar 15;59:1-8. Epub 2019 Mar 15.

Division of Inflammation Biology, La Jolla Institute for Immunology, La Jolla, CA 92037, USA; Institute of Arboviruses, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325000, China. Electronic address:

Zika and the four serotypes of dengue are closely related flaviviruses that share a high degree of structural and sequence homology and co-circulate in many regions of the world. Here, we review recent studies investigating antigenic cross-reactivity between the two viruses. We discuss the pathogenic and protective roles of cross-reactive anti-viral antibody and T cell responses, respectively, in modulating the outcome of secondary dengue or Zika infection. Read More

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http://dx.doi.org/10.1016/j.coi.2019.02.001DOI Listing
March 2019
1 Read

Dendritic cells are what they eat: how their metabolism shapes T helper cell polarization.

Curr Opin Immunol 2019 Mar 12;58:16-23. Epub 2019 Mar 12.

Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands. Electronic address:

Dendritic cells (DCs) are professional antigen-presenting cells that play a crucial role in the priming and differentiation of CD4 T cells into several distinct subsets including effector T helper (Th) 1, Th17 and Th2 cells, as well as regulatory T cells (Tregs). It is becoming increasingly clear that cellular metabolism shapes the functional properties of DCs. Specifically, the ability of DCs to drive polarization of different Th cell subsets may be orchestrated by the engagement of distinct metabolic pathways. Read More

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http://dx.doi.org/10.1016/j.coi.2019.02.003DOI Listing

What B cell memories are made of.

Curr Opin Immunol 2019 Mar 9;57:58-64. Epub 2019 Mar 9.

The Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, United States. Electronic address:

In many ways, memory B cells represent the ultimate outcome of humoral immunity. Many of these cells express exceptionally high affinity antigen-specific B cell receptors for antigen, and these cells are a critical source of the long-lived plasma cells that secrete protective serum antibodies to protect against secondary exposure to pathogens and other life-threatening antigens. Evidence is now emerging that not all memory B cells are created via the same cellular pathways and molecular events. Read More

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http://dx.doi.org/10.1016/j.coi.2019.01.003DOI Listing

New technologies and applications in infant B cell immunology.

Curr Opin Immunol 2019 Feb 27;57:53-57. Epub 2019 Feb 27.

Department of Pathology, Stanford School of Medicine, Stanford University, USA. Electronic address:

The human immune system changes dramatically with age, and early life exposures to pathogens and environmental antigens begin the formation of immune memory which influences subsequent responses later in life. To study infant immunity, sample-sparing experimental methods that extract maximal data from small samples of blood or other tissues are needed; fortunately, recent developments in high-throughput sequencing and multiplexed labeling and measurement of markers on cells are well-suited to these tasks. Here, we review some recent studies of infant immune responses to infectious disease, highlighting similarities and differences between infants and adults, and identifying important questions for future research. Read More

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http://dx.doi.org/10.1016/j.coi.2018.12.005DOI Listing
February 2019
1 Read

B cells in the formation of tertiary lymphoid organs in autoimmunity, transplantation and tumorigenesis.

Curr Opin Immunol 2019 Feb 21;57:46-52. Epub 2019 Feb 21.

Centre for Experimental Medicine & Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, UK. Electronic address:

Tertiary lymphoid organs named also tertiary lymphoid structures (TLS) often occur at sites of autoimmune inflammation, organ transplantation and cancer. Although the mechanisms for their formation/function are not entirely understood, it is known that TLS can display features of active germinal centres supporting the proliferation and differentiation of (auto)-reactive B cells. In this Review, we discuss current knowledge on TLS-associated B cells with particular reference on how within diseased tissues these structures are linked to either deleterious or protective outcomes in patients and the potential for therapeutic targeting of TLS through novel drugs. Read More

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http://dx.doi.org/10.1016/j.coi.2019.01.004DOI Listing
February 2019
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T-bet B cells: A common denominator in protective and autoreactive antibody responses?

Curr Opin Immunol 2019 Feb 19;57:40-45. Epub 2019 Feb 19.

Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

T-bet B cells have emerged as a key component of the humoral immune response in both infections and autoimmune disorders, with many of their phenotypic and functional attributes conserved between mice and humans. They are protective (infections) and pathogenic (autoimmunity), although the associated commonalities and differences remain unclear. Heterogeneity within this pool, in terms of origin, fate and function may underlie these divergent roles. Read More

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http://dx.doi.org/10.1016/j.coi.2019.01.002DOI Listing
February 2019
2 Reads

MHC I chaperone complexes shaping immunity.

Curr Opin Immunol 2019 Feb 14;58:9-15. Epub 2019 Feb 14.

Institute of Biochemistry, Biocenter, Goethe University Frankfurt, Max-von-Laue Str. 9, 60438 Frankfurt/Main, Germany. Electronic address:

Major histocompatibility complex class I (MHC I) molecules present peptides on the surface of most nucleated cells and allow the immune system to detect and eliminate infected or malignantly transformed cells. The peptides are derived from endogenous proteins by proteasomal degradation or aberrant translation, and are translocated from the cytosol into the endoplasmic reticulum (ER) by the transporter associated with antigen processing (TAP), a central component of the peptide-loading complex (PLC). The peptides are subsequently processed by ER-resident aminopeptidases (ERAP1/2) and loaded onto MHC I. Read More

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http://dx.doi.org/10.1016/j.coi.2019.01.001DOI Listing
February 2019

The labyrinth unfolds: architectural rearrangements of the endolysosomal system in antigen-presenting cells.

Curr Opin Immunol 2019 Feb 6;58:1-8. Epub 2019 Feb 6.

Oncode Institute, Department of Cell and Chemical Biology, Leiden University Medical Center, Einthovenweg 20, 2333 ZC, Leiden, The Netherlands. Electronic address:

Antigen-presenting cells (APCs) capture and present pathogens to T cells, thus arousing adaptive immune responses geared at the elimination of these invaders. In APCs, pathogens acquired from the extracellular space intersect with MHC class II (MHC-II) molecules in the endolysosomal system, where processing and loading of antigenic peptides occur. The resulting complexes can then be directed to the cell surface for recognition by T cells. Read More

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http://dx.doi.org/10.1016/j.coi.2018.12.004DOI Listing
February 2019
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Affinity war: forging immunoglobulin repertoires.

Curr Opin Immunol 2019 Jan 25;57:32-39. Epub 2019 Jan 25.

Department of Medicine, Division of Rheumatology, Immunology and Allergy Brigham and Women's Hospital and Harvard Medical School, USA. Electronic address:

B cell immunoglobulin (Ig) repertoire composition shapes immune responses. The generation of Ig diversity begins with Ig variable region exon assembly from gene segments, random inter-segment junction sequence diversity, and combinations of Ig heavy and light chain. This generates vast preemptive sequence freedom in early developing B lineage cell Ig genes that can anticipate a great diversity of threats. Read More

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http://dx.doi.org/10.1016/j.coi.2018.12.002DOI Listing
January 2019
1 Read

B-1 cell responses to infections.

Curr Opin Immunol 2019 Jan 24;57:23-31. Epub 2019 Jan 24.

Graduate Group in Integrative Pathobiology, University of California, Davis, United States; Center for Comparative Medicine, University of California, Davis, United States; Dept. Pathology, Microbiology & Immunology, School of Veterinary Medicine, University of California, Davis, United States. Electronic address:

B-1 cells represent an innate-like early-developing B cell population, whose existence as an independent lymphocyte subset has been questioned in the past. Recent molecular and lineage tracing studies have not only confirmed their unique origins and differentiation paths, they have also provided a rationale for their distinctive functionalities compared to conventional B cells. This review summarizes our current understanding of B-1 cell development, and the activation events that regulate B-1 cell responses to self and foreign antigens. Read More

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http://dx.doi.org/10.1016/j.coi.2018.12.001DOI Listing
January 2019
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Microbiome control of innate reactivity.

Curr Opin Immunol 2019 Feb 22;56:107-113. Epub 2019 Jan 22.

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.

Numerous scientific disciplines, including immunology, are now positioned to fully realize the potential of the intestinal microbiome to modulate a wide array of basic processes. Increasingly, microbiota-derived metabolites are being recognized for mediating these effects. Coupled with advances in large scale sequencing and mass spectrometry, research into the microbiota and their metabolites has entered into an era of rapid discovery. Read More

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http://dx.doi.org/10.1016/j.coi.2018.12.003DOI Listing
February 2019
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Cellular pathways in the development of human and murine innate lymphoid cells.

Curr Opin Immunol 2019 Feb 19;56:100-106. Epub 2018 Dec 19.

Department of Hematology, City of Hope National Medical Center, Los Angeles, CA, United States. Electronic address:

Innate lymphoid cells (ILCs) are critical to effective immune surveillance against pathogens, have malignant counterparts, and contribute to disease. Thus, it is important to understand ILC development. All ILCs are derived from the common lymphoid progenitor cell; however, the exact mechanisms and signals that initiate their divergence from T cells, B cells and one and other are incompletely understood. Read More

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http://dx.doi.org/10.1016/j.coi.2018.11.003DOI Listing
February 2019
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Editorial overview: Autoimmunity: A new frontier awaits.

Authors:
Daniel B Stetson

Curr Opin Immunol 2018 Dec;55:iii-iv

Department of Immunology, University of Washington School of Medicine, 750 Republican St, Seattle, WA 98109, USA. Electronic address:

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http://dx.doi.org/10.1016/j.coi.2018.11.005DOI Listing
December 2018
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Neuronal regulation of innate lymphoid cells.

Curr Opin Immunol 2019 Feb 7;56:94-99. Epub 2018 Dec 7.

Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY 10021, USA. Electronic address:

The cardinal signs of inflammation suggest a close connection between the nervous system and the immune system. However, the cellular and molecular basis of these interactions remains incompletely defined. Recent research has demonstrated that tissue-resident innate lymphoid cells (ILCs) obtain neuronal signals, particularly at mucosal barriers, where ILCs regulate tissue homeostasis. Read More

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http://dx.doi.org/10.1016/j.coi.2018.11.002DOI Listing
February 2019
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Innate lymphoid cell sensing of tissue vitality.

Curr Opin Immunol 2019 Feb 5;56:82-93. Epub 2018 Dec 5.

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, United States. Electronic address:

Innate lymphoid cells (ILCs) constitute a heterogeneous population of cytokine-secreting cells that colonize different tissues and are heavily reliant on cytokines and other secreted factors for their development, maintenance and effector functions. Most ILCs are tissue resident and differentiate in non-lymphoid peripheral tissues. As tissue-resident sentinels, ILCs must rapidly identify pathogens or malignancy in an effort to return the tissue to homeostasis. Read More

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http://dx.doi.org/10.1016/j.coi.2018.11.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6469350PMC
February 2019
1 Read

ILC2s - resident lymphocytes pre-adapted to a specific tissue or migratory effectors that adapt to where they move?

Curr Opin Immunol 2019 Feb 23;56:76-81. Epub 2018 Nov 23.

Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Electronic address:

A cardinal feature of the T-cell adaptive immune system is the antigen-dependent activation of naïve T cells in secondary lymphoid sites, followed by the migration of the resultant effector cells through the efferent lymph to the blood and then into a peripheral tissue site of infection or tumor growth. In contrast, the current view of innate lymphocytes (ILCs), the innate counterparts of T cells, is that they are tissue-resident cells, adapted to their specific environments during development and performing their effector functions locally upon cytokine stimulation. Here we present recent findings that challenge the latter as defining the properties of ILCs, at least ILC2s. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S09527915183006
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http://dx.doi.org/10.1016/j.coi.2018.11.001DOI Listing
February 2019
9 Reads

Updates on autoinflammatory diseases.

Curr Opin Immunol 2018 Dec 16;55:97-105. Epub 2018 Nov 16.

Translational Autoinflammatory Diseases Section, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA. Electronic address:

Autoinflammatory diseases are hyperinflammatory, immune dysregulatory diseases caused by innate immune cells dysregulation that present typically in the perinatal period with systemic and organ-targeted inflammation, but with improved genetic testing and the development of diagnostic criteria, milder and later-onset forms are being detected in adulthood. While the discovery of gain-of-function mutations in innate sensors linked to the production of proinflammatory cytokines provided the bases for anti-cytokine therapies that changed disease and patient outcomes, the field is expanding with the increasing discovery of disease-causing loss-of-function mutations in genes with cellular house-keeping functions that affect cell homeostasis and when dysregulated trigger innate inflammatory pathways. This review focuses on updates on molecular pathways and diseases that cause predominantly IL-1β and Type-I IFN-mediated autoinflammatory diseases. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.014DOI Listing
December 2018
14 Reads

Bridging the gap between vaccination with Bacille Calmette-Guérin (BCG) and immunological tolerance: the cases of type 1 diabetes and multiple sclerosis.

Curr Opin Immunol 2018 Dec 15;55:89-96. Epub 2018 Nov 15.

Center for Experimental Neurological Therapies, Sant'Andrea Hospital, Department of Neurosciences, Mental Health and Sensory Organs, Sapienza University of Rome, S. Andrea Hospital, Via di Grottarossa 1035, 00189 Rome, Italy; IRCCS Istituto Neurologico Mediterraneo (INM) Neuromed, 86077 Pozzilli, IS, Italy. Electronic address:

At the end of past century, when the prevailing view was that treatment of autoimmunity required immune suppression, experimental evidence suggested an approach of immune-stimulation such as with the BCG vaccine in type 1 diabetes (T1D) and multiple sclerosis (MS). Translating these basic studies into clinical trials, we showed the following: BCG harnessed the immune system to 'permanently' lower blood sugar, even in advanced T1D; BCG appeared to delay the disease progression in early MS; the effects were long-lasting (years after vaccination) in both diseases. The recently demonstrated capacity of BCG to boost glycolysis may explain both the improvement of metabolic indexes in T1D, and the more efficient generation of inducible regulatory T cells, which counteract the autoimmune attack and foster repair mechanisms. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.016DOI Listing
December 2018
7 Reads

Lambda interferons come to light: dual function cytokines mediating antiviral immunity and damage control.

Curr Opin Immunol 2019 Feb 3;56:67-75. Epub 2018 Nov 3.

Laboratory of Immunobiology, Center for Clinical, Experimental Surgery and Translational Research, Biomedical Research Foundation of the Academy of Athens, 11527 Athens, Greece.

Lambda interferons (IFNλs, type III IFNs or interleukins-28/29) were described fifteen years ago as novel cytokines sharing structural and functional homology with IL-10 and type I IFNs, respectively. IFNλs engage a unique receptor complex comprising IFNLR1 and IL10R2, nevertheless they share signaling cascade and many functions with type I IFNs, questioning their possible non-redundant roles and overall biological importance. Here, we review the latest evidence establishing the primacy of IFNλs in front line protection at anatomical barriers, mediating antiviral immunity before type I IFNs. Read More

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http://dx.doi.org/10.1016/j.coi.2018.10.007DOI Listing
February 2019
2 Reads

The long and the short of it: insights into the cellular source of autoantibodies as revealed by B cell depletion therapy.

Curr Opin Immunol 2018 Dec 1;55:81-88. Epub 2018 Nov 1.

Seattle Children's Research Institute, Seattle, WA, United States; Department of Pediatrics, University of Washington, School of Medicine, United States. Electronic address:

High titers of pathogenic autoantibodies are a hallmark of many autoimmune diseases. However, much remains unknown about the self-reactive plasma cells that are key mediators of disease. We propose a model in which the varying efficacy of precursor B cell depletion for the treatment of humoral autoimmunity can be explained by differences in the relative contributions of pathogenic antibodies by short-lived versus long-lived plasma cells. Read More

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http://dx.doi.org/10.1016/j.coi.2018.10.008DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6289281PMC
December 2018
13 Reads

Age (autoimmunity) associated B cells (ABCs) and their relatives.

Curr Opin Immunol 2018 Dec 31;55:75-80. Epub 2018 Oct 31.

Department of Biomedical Research, National Jewish Health, 1400, Jackson St., Denver, CO 80206, USA; Department of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA. Electronic address:

B cells affect human and animal health in numerous ways. They are the precursors for the antibody-secreting plasma cells and they also take up antigen, particularly antigen for which they bear-specific receptors, very efficiently and thus present antigen to T cells. The T cell-B cell interactions that thus occur serve not only to affect the B cell, but also, the T cell partner of the interaction. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.007DOI Listing
December 2018
1 Read

Dead or alive: how the immune system detects microbial viability.

Curr Opin Immunol 2019 Feb 24;56:60-66. Epub 2018 Oct 24.

Department of Infectious Diseases and Pulmonary Medicine, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany; German Center for Lung Research (DZL), Berlin, Germany. Electronic address:

Immune detection of microbial viability is increasingly recognized as a potent driver of innate and adaptive immune responses. Here we describe recent mechanistic insights into the process of how the immune system discriminates between viable and non-viable microbial matter. Accumulating evidence suggests a key role for microbial RNA as a widely conserved viability associated PAMP (vita-PAMP) and a molecular signal of increased infectious threat. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.018DOI Listing
February 2019
17 Reads

Antiviral resistance of stem cells.

Curr Opin Immunol 2019 Feb 20;56:50-59. Epub 2018 Oct 20.

Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY 10065, United States. Electronic address:

Stem cells are important for growth and regeneration given their ability to self-renew and differentiate into mature cells. Resistance to certain viral infections has been established as a phenotype of stem cells, a protection in line with their important physiological function. Antiviral resistance is critical to all cells, but it is differentially regulated between stem cells and differentiated cells. Read More

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http://dx.doi.org/10.1016/j.coi.2018.10.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6462420PMC
February 2019
16 Reads

Editorial overview: Tuning the innate immune response to pathogens.

Curr Opin Immunol 2018 10;54:vi-ix

Department of Immunology and Microbiology, University of Colorado School of Medicine, United States.

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http://dx.doi.org/10.1016/j.coi.2018.10.001DOI Listing
October 2018
3 Reads

Editorial overview: Allergy and hypersensitivity: Emerging concepts in allergy and type 2 immunity.

Curr Opin Immunol 2018 10;54:iii-v

Institute of Pathology, Division of Experimental Pathology, University of Bern, 3008 Bern, Switzerland. Electronic address:

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http://dx.doi.org/10.1016/j.coi.2018.10.002DOI Listing
October 2018
1 Read

Innate immune priming of insulin secretion.

Authors:
Elise Dalmas

Curr Opin Immunol 2019 Feb 18;56:44-49. Epub 2018 Oct 18.

French Institute for Health and Medical Research (INSERM), Cordeliers Research Center UMR_S 1138, Sorbonne Paris Cité, Paris Descartes University, Paris Diderot University, Paris, France. Electronic address:

Increasing evidence suggests a role for the immune system to finely tune metabolic homeostasis. The possibility that the immune system can likewise regulate islet endocrine function has only commenced drawing attention. Islet beta cells are the main producers of insulin and have to dynamically respond to fluctuating insulin demands of the body. Read More

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http://dx.doi.org/10.1016/j.coi.2018.10.005DOI Listing
February 2019
12 Reads

Oxeiptosis: a discreet way to respond to radicals.

Curr Opin Immunol 2019 Feb 18;56:37-43. Epub 2018 Oct 18.

Immunopathology of Virus Infections, Institute of Virology, Technical University of Munich, Schneckenburger Str. 8, 81675 Munich, Germany; German Center for Infection Research (DZIF), Munich Partner Site, Germany. Electronic address:

One of the best-studied cellular responses to toxic signals and pathogens is programmed cell death. Over the past years, it became apparent that the specific mechanisms of cell death have tremendous influence at both cellular and organismal level, highlighting the importance of sensors and pathways involved in this decision-making process. Central signalling molecules involved in a variety of cell death pathways are reactive oxygen species (ROS). Read More

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http://dx.doi.org/10.1016/j.coi.2018.10.006DOI Listing
February 2019
18 Reads

Epigenetic dynamics in normal and malignant B cells: die a hero or live to become a villain.

Curr Opin Immunol 2018 Oct 17;57:15-22. Epub 2018 Oct 17.

Department of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO 63110, USA. Electronic address:

Normal B cell development, activation, and terminal differentiation depend on the intricate dynamics of cooperating epigenetic and non-coding components to control the level and timing of expression of thousands of genes. Recent genome-wide studies have integratively mapped changes in the chromatin landscape, DNA methylome, 3-dimensional interactome, and coding and non-coding transcriptomes of normal and malignant B cells. Genetic ablation in human cells and mouse models has begun to elucidate the coordinated roles of essential epigenetic modifiers, key transcription factors, and long non-coding RNAs in B cell biology. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.020DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6470061PMC
October 2018
6 Reads

Regulation of metabolic supply and demand during B cell activation and subsequent differentiation.

Curr Opin Immunol 2018 Oct 16;57:8-14. Epub 2018 Oct 16.

Department of Immunobiology, University of Arizona College of Medicine, Tucson, AZ 85724, USA. Electronic address:

B cell activation and differentiation are associated with marked changes in proliferative and effector functions. Each stage of B cell differentiation thus has unique metabolic demands. New studies have provided insight on how nutrient uptake and usage by B cells are regulated by B cell receptor signals, autophagy, mammalian target of rapamycin, and transcriptional control of transporters and rate-limiting enzymes. Read More

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http://dx.doi.org/10.1016/j.coi.2018.10.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6467717PMC
October 2018
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From zero to sixty and back to zero again: the metabolic life of B cells.

Curr Opin Immunol 2018 Oct 9;57:1-7. Epub 2018 Oct 9.

Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA. Electronic address:

Throughout their lifetimes B cells shift metabolic gears to move rapidly from quiescent states to full out proliferative expansion and back again. Here we discuss recent findings that shed light on how B cells rapidly shift gears to metabolically fuel expansion and then just as rapidly down shift during phases of receptor rearrangements to ensure genome stability. We also discuss the link between metabolic activity and fate decisions in B cells. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.019DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456432PMC
October 2018
2 Reads

Innate immunosensing of DNA in cellular senescence.

Curr Opin Immunol 2019 Feb 5;56:31-36. Epub 2018 Oct 5.

Global Health Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Switzerland. Electronic address:

Senescence is a multistep cellular program featuring a stable cell cycle arrest, which occurs upon exposure to various stressors. Senescent cells exhibit metabolic activity and hypertrophy and produce a multitude of factors with both cell intrinsic as well as non-cell autonomous functions. These factors are collectively referred to as the senescence-associated secretory phenotype (SASP). Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.013DOI Listing
February 2019
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Control of autoreactive B cells by IgM and IgD B cell receptors: maintaining a fine balance.

Curr Opin Immunol 2018 Dec 5;55:67-74. Epub 2018 Oct 5.

Rosalind Russell and Ephraim P. Engleman Arthritis Research Center, Division of Rheumatology, Department of Medicine, University of California, San Francisco, CA, 94143, USA. Electronic address:

A substantial fraction of mature naïve B cells recognize endogenous antigens, and this autoreactivity must be controlled to prevent autoantibody secretion. Selective downregulation of the IgM BCR on autoreactive B cells has long been appreciated, and recent findings illustrate how this might impose tolerance. The BCR isotype maintained on autoreactive B cells, IgD, is less sensitive to endogenous antigens than IgM. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6291015PMC
December 2018
18 Reads

SAMHD1 and the innate immune response to cytosolic DNA during DNA replication.

Curr Opin Immunol 2019 Feb 5;56:24-30. Epub 2018 Oct 5.

Institut de Génétique Humaine, CNRS, Université de Montpellier, Equipe Labellisée Ligue contre le Cancer, Montpellier France. Electronic address:

Cytosolic DNA of endogenous or exogenous origin is sensed by the cGAS-STING pathway to activate innate immune responses. Besides microbial DNA, this pathway detects self-DNA in the cytoplasm of damaged or abnormal cells and plays a central role in antitumor immunity. The mechanism by which cytosolic DNA accumulates under genotoxic stress conditions is currently unclear, but recent studies on factors mutated in the Aicardi-Goutières syndrome cells, such as SAMHD1, RNase H2 and TREX1, are shedding new light on this key process. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.017DOI Listing
February 2019
21 Reads

Natural regulatory plasma cells.

Authors:
Simon Fillatreau

Curr Opin Immunol 2018 Dec 4;55:62-66. Epub 2018 Oct 4.

Institut Necker-Enfants Malades, INSERM U1151-CNRS UMR 8253, Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, Paris, France; AP-HP, Hôpital Necker Enfants Malades, Paris, France. Electronic address:

B cells can generate several types of antibody-secreting cells, including plasmablasts that divide and are short lived, as well as plasma cells that do not proliferate and can persist for extended time periods. Here, we discuss the identification of a novel subset of non-dividing plasma cells specialized in the production of interleukin(IL)-10. These cells develop at steady state, including in germ-free mice, via a mechanism dependent on the B cell receptor for antigen and possibly involving the recognition of damaged cells. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6290076PMC
December 2018
3 Reads

Reprogramming of mitochondrial metabolism by innate immunity.

Authors:
Johan Garaude

Curr Opin Immunol 2019 Feb 1;56:17-23. Epub 2018 Oct 1.

INSERM U1211, Rares Diseases: Genetics and Metabolism, University of Bordeaux, CHU Pellegrin, École de Sages-Femmes, 33000 Bordeaux, France. Electronic address:

The reprogramming of cellular metabolism has emerged as a major aspect of innate immune cell activation. Mitochondria, which are well known for their critical functions in cellular bioenergetics and metabolism, also serve innate immune purposes by providing specific signaling platforms. Latest advances in our understanding of innate immune receptor-mediated metabolic reprogramming have unraveled specific immune functions of mitochondrial metabolites that place mitochondrial metabolism and particularly the mitochondrial respiratory chain at the center of innate immunity. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.010DOI Listing
February 2019
17 Reads

LAP it up, fuzz ball: a short history of LC3-associated phagocytosis.

Curr Opin Immunol 2018 Dec 2;55:54-61. Epub 2018 Oct 2.

Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, NC, USA. Electronic address:

LC3-associated phagocytosis (LAP) exists at the crossroads of the two evolutionary pathways of phagocytosis and autophagy. When a phagocyte engulfs an extracellular particle that engages receptor signaling, components of the autophagy machinery and Rubicon are recruited to the cargo-containing phagosome or LAPosome. Formation of the LAPosome is critical for both cargo clearance as well as mediating the proper signaling cascade. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.011DOI Listing
December 2018
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Coagulopathies and inflammatory diseases: '…glimpse of a Snark'.

Curr Opin Immunol 2018 Dec 27;55:44-53. Epub 2018 Sep 27.

Department of Immunobiology, School of Medicine, Yale University, 300 Cedar Street, New Haven, CT 06520, United States; Department of Pharmacology, School of Medicine, Yale University, 333 Cedar Street, New Haven, CT 06520, United States. Electronic address:

Coagulopathies and inflammatory diseases, ostensibly, have distinct underlying molecular bases. Notwithstanding, both are host defense mechanisms to physical injury. In invertebrates, clotting can function directly in anti-pathogen defense. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6366937PMC
December 2018
20 Reads

Regulation of lymphocyte trafficking in central nervous system autoimmunity.

Curr Opin Immunol 2018 Dec 27;55:38-43. Epub 2018 Sep 27.

Benaroya Research Institute at Virginia Mason, Immunology Program, Seattle, WA, 98101, USA; University of Washington, Department of Immunology, Seattle, WA, 98105, USA. Electronic address:

CD4 T helper (Th) cells play a central role in orchestrating protective immunity but also in autoimmunity. Multiple Sclerosis (MS) is a human autoimmune disease of the central nervous system (CNS) characterized by the infiltration of inflammatory lymphocytes and myeloid cells into the brain and spinal cord, leading to demyelination, axonal damage, and progressive loss of motor functions. The release of T cells in the circulation and their migration in the central nervous system are key and tightly regulated processes which have been targeted to decrease CD4 T cell presence in the CNS and limit disease progression. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.008DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6286213PMC
December 2018
1 Read

DNA as a self-antigen: nature and regulation.

Curr Opin Immunol 2018 Dec 24;55:31-37. Epub 2018 Sep 24.

Department of Pathology, New York University School of Medicine, New York, NY 10016, USA; Department of Medicine, New York University School of Medicine, New York, NY 10016, USA. Electronic address:

High-affinity antibodies to double-stranded DNA are a hallmark of systemic lupus erythematosus (SLE) and are thought to contribute to disease flares and tissue inflammation such as nephritis. Notwithstanding their clinical importance, major questions remain about the development and regulation of these pathogenic anti-DNA responses. These include the mechanisms that prevent anti-DNA responses in healthy subjects, despite the constant generation of self-DNA and the abundance of DNA-reactive B cells; the nature and physical form of antigenic DNA in SLE; the regulation of DNA availability as an antigen; and potential therapeutic strategies targeting the pathogenic DNA in SLE. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6317730PMC
December 2018
14 Reads

IL-6: a cytokine at the crossroads of autoimmunity.

Curr Opin Immunol 2018 Dec 21;55:9-14. Epub 2018 Sep 21.

Translational Research Program, Benaroya Research Institute, Seattle, WA, 98101, USA. Electronic address:

IL-6 is implicated in the development and progression of autoimmune diseases in part by influencing CD4 T cell lineage and regulation. Elevated IL-6 levels drive inflammation in a wide range of autoimmune diseases, some of which are also characterized by enhanced T cell responses to IL-6. Notably, the impact of IL-6 on inflammation is contextual in nature and dependent on the cell type, cytokine milieu and tissue. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6286200PMC
December 2018
1 Read

Extracellular matrix and the maintenance and loss of peripheral immune tolerance in autoimmune insulitis.

Curr Opin Immunol 2018 Dec 22;55:22-30. Epub 2018 Sep 22.

Division of Infectious Diseases and Geographic Medicine, Dept. of Medicine, Stanford University School of Medicine, Beckman Center, 279 Campus Drive, Stanford, CA, 94305, United States. Electronic address:

There is a growing appreciation that the extracellular matrix (ECM) contributes to both the maintenance of immune tolerance in healthy tissues and to its loss at sites of autoimmunity. Here, we review recent literature on the role of ECM and particularly the glycosaminoglycans hyaluronan and heparan sulfate in the development of autoimmune, type 1 diabetes (T1D). Data from transplant models suggest that healthy islets are embedded within an intact ECM that supports beta-cell homeostasis and provides physical and immunoregulatory barriers against immune infiltration. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6286219PMC
December 2018
2 Reads

Microbiota - an amplifier of autoimmunity.

Curr Opin Immunol 2018 Dec 22;55:15-21. Epub 2018 Sep 22.

Laboratory for Mucosal Immunity, Center for Integrative Medical Sciences, RIKEN Yokohama Institute, Tsurumi Ward, Suehirocho, 1 Chome-7-22, Yokohama, Kanagawa Prefecture, 230-0045, Japan. Electronic address:

Many studies describe dysbiosis as a change in the microbiota that accompanies autoimmune illnesses, but little is known about whether these changes are a cause or consequence of an altered immune state. The immune system actively shapes the composition of the microbiota, with divergent outcomes in healthy or autoimmune-prone individuals. The gut microbiota in turn acts as an acquired endocrine organ, influencing the physiology of the host via release of nutrients and chemical messengers. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.003DOI Listing
December 2018
14 Reads

Emerging areas for therapeutic discovery in SLE.

Curr Opin Immunol 2018 Dec 21;55:1-8. Epub 2018 Sep 21.

Center for Autoimmunity, Musculoskeletal and Hematologic Diseases, Feinstein Institute for Medical Research, Manhasset, New York, NY 11030, United States. Electronic address:

Recent advances in the field of autoimmunity have identified numerous dysfunctional pathways in Systemic Lupus Erythematosus (SLE), including aberrant clearance of nucleic-acid-containing debris and immune complexes, excessive innate immune activation leading to overactive type I IFN signalling, and abnormal B and T cell activation. On the background of genetic polymorphisms that reset thresholds for immune responses, multiple immune cells contribute to inflammatory amplification circuits. Neutrophils activated by immune complexes are a rich source of immunogenic nucleic acids. Read More

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http://dx.doi.org/10.1016/j.coi.2018.09.004DOI Listing
December 2018
4 Reads