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Platelets as immune cells in physiology and immunopathology

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197408 Year: Pages: 111 DOI: 10.3389/978-2-88919-740-8 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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Are platelets cells? (Not everyone agrees, since they are non-nucleate). And if platelets are cells - which all specialists consider at the time being - are they immune cells? The issue that platelets participate in immunity is no longer debated; however, the issue that they are key cells in immunity is challenged. It has even been proposed a couple of years ago that platelets can present antigen to T-lymphocytes by using their HLA class I molecules. No one has the same functional definition of platelets. The ‘Frontiers Research Topic’- coordinators’ own view is that platelets are primarily repairing cells, what they do in deploying tools of physiological inflammation. This function is better acknowledged as primary hemostasis, i.e. platelet adherence to injured or wounded vessels, followed by activation, aggregation, and constitution of the initial clot. Platelets would thus repair damaged vascular endothelium; so doing, as they patrol to detect damages, they sense danger along the vascular arborescence. As the latter is immense, platelets get close to tissues, which are not allowed to them under ‘physiological’ conditions but are readily accessible in pathology. Platelets are equipped with a variety of Pathogen Recognition Receptors such as TLRs; they have a complete signalosome, which is functional until the phosphorylation of NFkB; they have been proved to retro-transcribe RNA and synthesize de novo proteins; etc. Platelets participate to inflammation along the whole spectrum: from physiological (tissue repair, healing) to acute/severe inflammation (as can be seen in e.g. sepsis). In general, platelets engage complex interactions with most infectious pathogens. We propose there to cover those topics - from physiology to pathology, that put platelets within cells that not only take place in-, but also are key players of-, innate immunity. The relation of platelets with adaptive immunity is even more complex. Not everyone is convinced that platelets present antigens; however, platelets influence adaptive immunity since they have mutual interactions with Dendritic cells, Monocytes/Macrophages, and B-lymphocytes (the key players of antigen presentation); they also have mutual interactions with T-lymphocytes, though is issue is less clearly deciphered. We propose to also cover these topics - or to present the forum. There is another issue which is medically relevant - speaking of physiology/physiopathology-: this is fetal maternal incompatibility of platelet specific antigens (the HPA system) and the likely formation of maternal antibodies that often injure the newborn with risks of severe thrombocytopenia and intracranial hemorrhage. We propose an update on this issue as well. Last, platelets are very special because they can be directly therapeutic (by transfusion), even when being offered by a generous blood donor displaying given genetic and phenotypic parameters to a patient/recipient in need, who also display his/her own genetic and phenotypic parameters, which - for a large part - differ from the donor's ones. Besides immunization - via mechanisms probably close to the fetal maternal platelet incompatibility, but likely not similar -, transfusion has allowed the identification of the tremendous capacity of platelets to mediate inflammation: we propose to conclude the Topics with this item/forum.

Keywords

platelets --- Infection --- Inflammation --- immunity

Comparative studies between HTLV-1 and HTLV-2 function and pathobiology

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194988 Year: Pages: 94 DOI: 10.3389/978-2-88919-498-8 Language: English
Publisher: Frontiers Media SA
Subject: Microbiology --- Science (General)
Added to DOAB on : 2015-11-16 15:44:59
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Human T-cell leukemia viruses type 1 and 2 (HTLV-1 and HTLV-2) share a common genetic organization, expression strategy and ability to infect and immortalize T-cells in vitro; however, HTLV-1 and HTLV-2 are strikingly different in terms of clinical impact. HTLV-1 is recognized as the aetiological agent of adult T-cell leukemia/lymphoma (ATLL), and HTLV-associated myeolopathy/tropical spastic paraparesis (HAM/TSP), in contrast, HTLV-2 does not cause hematologic disorders and is only sporadically associated with cases of subacute myelopathy. HTLV-1 and HTLV-2 also exhibit distinct cellular tropisms in vivo: HTLV-1 is mainly found in CD4+T lymphocytes, whereas CD8+T-cells are the preferred target for HTLV-2. The articles contributed in this Research Topic are covering all the different aspects that characterize HTLV-1 and HTLV-2, by highlighting differences in their biology that might provide clues to their distinct pathogenic properties.

Keywords

HTLV-1 --- HTLV-2 --- Expression --- Proteins --- Co-infection

M1/M2 Macrophages: The Arginine Fork in the Road to Health and Disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194995 Year: Pages: 280 DOI: 10.3389/978-2-88919-499-5 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2015-12-03 13:02:24
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Macrophages have unique and diverse functions necessary for survival. And, in humans (and other species), they are the most abundant leukocytes in tissues. The Innate functions of macrophages that are best known are their unusual ability to either "Kill" or "Repair". Since killing is a destructive process and repair is a constructive process, it was stupefying how one cell could exhibit these 2 polar – opposite functions. However, in the late 1980’s, it was shown that macrophages have a unique ability to enzymatically metabolize Arginine to Nitric Oxide (NO, a gaseous non – specific killer molecule) or to Ornithine (a precursor of polyamines and collagen for repair). The dual Arginine metabolic capacity of macrophages provided a functional explanation for their ability to kill or repair. Macrophages predominantly producing NO are called M1 and those producing Ornithine are called M2. M1 and M2 – dominant responses occur in lower vertebrates, and in T cell deficient vertebrates being directly driven by Damage and Pathogen Associated Molecular Patterns (DAMP and PAMP). Thus, M1 and M2 are Innate responses that protect the host without Adaptive Immunity. In turn, M1/M2 is supplanting previous models in which T cells were necessary to "activate" or "alternatively activate" macrophages (the Th1/Th2 paradigm). M1 and M2 macrophages were named such because of the additional key findings that these macrophages stimulate Th1 and Th2 – like responses, respectively. So, in addition to their unique ability to kill or repair, macrophages also govern Adaptive Immunity. All of the foregoing would be less important if M1 or M2 – dominant responses were not observed in disease. But, they are. The best example to date is the predominance of M2 macrophages in human tumors where they act like wound repair macrophages and actively promote growth. More generally, humans have become M2 – dominant because sanitation, antibiotics and vaccines have lessened M1 responses. And, M2 dominance seems the cause of ever - increasing allergies in developed countries. Obesity represents a new and different circumstance. Surfeit energy (e.g., lipoproteins) causes monocytes to become M1 dominant in the vessel walls causing plaques. Because M1 or M2 dominant responses are clearly causative in many modern diseases, there is great potential in developing the means to selectively stimulate (or inhibit) either M1 or M2 responses to kill or repair, or to stimulate Th1 or Th2 responses, depending on the circumstance. The contributions here are meant to describe diseases of M1 or M2 dominance, and promising new methodologies to modulate the fungible metabolic machinery of macrophages for better health.

Keywords

macrophage --- innate immunity --- M1 --- M2 --- wound --- Cancer --- Infection --- Atherosclerosis

The Neonatal Immune System: A Unique Host-Microbial Interface

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889454037 Year: Pages: 175 DOI: 10.3389/978-2-88945-403-7 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Pediatrics --- Allergy and Immunology --- Science (General) --- Microbiology
Added to DOAB on : 2018-11-16 17:17:57
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Emerging from the protective environment of the uterus, the newborn is exposed to a myriad of microbes, and quickly establishes a complex microbiome that shapes the infant’s biology in ways that are only now beginning to come to light. Among these exposures are a number of potential pathogens. The host responses to these pathogens in the neonatal period are unique, reflecting a developing immune system even with delivery at term. Preterm infants are delivered at a time when host defense mechanisms are even less developed and therefore face additional risk. As such, the organisms that cause disease in this period are different from the pathogens that are common in other age groups, or the disease they cause manifests in more severe fashion. Developmental alterations in both innate and adaptive immune responses in neonates have been documented among many cell types and pathways over the last several decades. Contemporary insights into the human immune system and methodologies that allow an “omics” approach to these questions have continued to provide new information regarding the mechanisms that underlie the human neonate as an “immunocompromised host.” This Research Topic highlights studies related to this unique host-pathogen interface. Contributions include those related to the innate or adaptive immune system of neonates, their response to microbial colonization or infection, and/or the pathogenesis of microbes causing disease in neonates.

The Role of Iron in Bacterial Pathogenesis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456628 Year: Pages: 156 DOI: 10.3389/978-2-88945-662-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Internal medicine
Added to DOAB on : 2019-01-23 14:53:43
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The collection of articles published in this eBook represent different facets of the interactions between pathogens and their host concerning the battle for iron. Pathogens have developed different strategies to acquire iron from their host. These include the production of siderophores, heme acquisition and ferrous iron uptake.

Structural and computational glycobiology: immunity and infection

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196388 Year: Pages: 102 DOI: 10.3389/978-2-88919-638-8 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2015-10-30 16:33:44
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Interest in understanding the biological role of carbohydrates has increased significantly over the last 20 years. The use of structural techniques to understand carbohydrate-protein recognition is still a relatively young area, but one that is of emerging importance. The high flexibility of carbohydrates significantly complicates the determination of high quality structures of their complexes with proteins. Specialized techniques are often required to understand the complexity of carbohydrate recognition by proteins. In this Research Topic, we will focus on structural and computational approaches to understanding carbohydrate recognition by proteins involved in immunity and infection. Particular areas of focus include cancer immunotherapeutics, carbohydrate-lectin interactions, glycosylation and glycosyltransferases.

CD4+ T cell differentiation in infection: amendments to the Th1/Th2 axiom

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195657 Year: Pages: 111 DOI: 10.3389/978-2-88919-565-7 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-01-19 14:05:46
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CD4+ T lymphocytes play an essential role in host defense against bacterial, parasitic and viral infections. During infection, under the influence of intrinsic signals received through peptide-MHC/TCR interactions and extrinsic signals provided by pathogen-conditioned dendritic and other accessory cells, CD4+ T cells proliferate and differentiate into specialized T helper (Th) effectors, which produce distinct sets of cytokines tailored to combat a specific class of microbes. The concept of CD4+ T cell multi-functionality was developed after the seminal discovery of Th1 and Th2 cells nearly 30 years ago. Although the Th1/Th2 paradigm has successfully withstood the test of time, in the past decade additional Th subsets (Th17, Tfh, Th22, Th9) have been identified. Similarly, single cell analyses of cytokines and master transcriptional factors have revealed that, at the population level, CD4+ T cell responses are far more heterogeneous than initially anticipated. While some of the checkpoints in Th cell specification have been identified, recent studies of transcriptional and epigenetic regulation have uncovered a significant flexibility during the course CD4+ T lymphocyte polarization. In addition, Th cells expressing cytokines with counteracting functions, as a measure of self-regulation, display yet another level of diversity. Understanding the mechanisms that control the balance between stability vs. plasticity of Th effectors both at the time of initiation of immune response and during development of CD4 T cell memory is critical for the rational design of better vaccines and new immunotherapeutic strategies. This research topic will cover current views on Th cell development, with a focus on the mechanisms that govern differentiation, function and regulation of effector Th cells in the context of microbial infections.

Toll-Like Receptor Activation in Immunity vs. Tolerance

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196364 Year: Pages: 75 DOI: 10.3389/978-2-88919-636-4 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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The innate immune system has evolved means to recognize and react suitably to foreign entities such as infectious agents. In many cases infectious microorganisms threaten the integrity and function of the target organs or tissues; therefore, consequent to their recognition the immune system becomes activated to ensure their elimination. Toll-like receptors (TLR) constitute a family of receptors specialized in the recognition of molecular patterns typically associated with infectious agents. Different TLRs exist, each selective for molecular entities and motifs belonging to a specific pathogen group. Consequently, it is thought that the molecular nature of invading microorganisms activates specific TLRs to drive adequate anti-infectious immunity. For instance, nucleic acid-specific, intracellular receptors (TLR3/7/8/9) are used to sense viruses and drive antiviral immunity, while other receptors (such as TLR2 and TLR4) recognize and promote immunity against bacteria, yeast, and fungi. Yet, it is becoming evident that activation of TLR pathways trigger mechanisms that not only stimulate but also regulate the immune system. For instance, TLR stimulation by viruses will drive antiviral interferon but also immunoregulatory cytokine production and regulatory T cell activation. Stimulation of TLRs by bacteria or using molecular agonists can also trigger both immune stimulatory and regulatory responses. TLR stimulation by infectious agents likely serves to activate but also control anti-infectious immunity, for instance prevent potential immunopathological tissue damage which can be caused by acute immune defense mechanisms. Previous work by us and others has shown that the immunoregulatory arm of TLR stimulation can additionally help control autoreactive processes in autoimmune disease. Hence, it is becoming established that gut commensals, which also play a crucial part in the control of autoimmune disease, establish immune regulatory mechanisms through activation of particular TLRs. In sum, it appears that TLRs are key immune players that not only stimulate but also regulate immune processes in health and disease. In this Research Topic, we wish to review the dual role of TLRs as activators and regulators of immune responses. We aim to motivate data-driven opinions as to the importance of context of TLR agonism for determining immune activation vs. regulation. The presentation of ongoing original works, as well as data and opinions around other innate immune receptors pertaining to this topic, are also encouraged.

CD1- and MR1-restricted T Cells in Antimicrobial Immunity

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197507 Year: Pages: 189 DOI: 10.3389/978-2-88919-750-7 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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Cell-mediated immunity to extracellular and intracellular microbes has been traditionally linked to CD4+ and CD8+ T cells that recognize pathogen-derived peptides in the context of major histocompatibility complex (MHC) class II and class I molecules, respectively. Recent progress in our understanding of early host defense mechanisms has brought ‘unconventional’, innate-like T cells into the spotlight. These are a heterogeneous population of non-MHC-restricted T cells that exhibit ‘memory-like’ properties and mount emergency responses to infection. They may directly detect and destroy infected cells, but are best known for their ability to regulate downstream effector cells including but not limited to conventional T cells. Innate-like T cells include among others CD1-restricted natural killer T (NKT) cells and MR1-restricted mucosa-associated invariant T (MAIT) cells. NKT cells recognize lipid antigens, and MAIT cells were recently demonstrated to respond to microbe-derived vitamin B metabolites. However, much remains to be learned about the antigen specificity range of these cells, their activation mode and their true potentials in immunotherapeutic applications. Like in many other areas of biology, uncertainties and controversies surrounding these cells and some of the experimental models, techniques and reagents employed to study them have brought about excitement and sometimes hot debates. This Special Topic was launched to provide updated reviews on protective and/or pathogenic roles of NKT and MAIT cells during infection. Leading experts discuss current controversies, pressing questions and the challenges that lie ahead for the advancement of this intriguing and rapidly evolving area of immunology. Unlike MHC, CD1 and MR1 display very limited polymorphism. Therefore, NKT and MAIT cells may be considered attractive targets for various diseases in diverse human populations. The potential benefits of NKT cell- and MAIT cell-based vaccination and treatment strategies in infectious diseases is an important subject that is also covered in this Topic.

Recent advances in γδ T cell biology: New ligands, new functions, and new translational perspectives

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197842 Year: Pages: 269 DOI: 10.3389/978-2-88919-784-2 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2016-04-07 11:22:02
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Gamma/delta (γδ) T-cells are a small subset of T-lymphocytes in the peripheral circulation but constitute a major T-cell population at other anatomical localizations such as the epithelial tissues. In contrast to conventional a/ß T-cells, the available number of germline genes coding for T-cell receptor (TCR) variable elements of γδ T-cells is very small. Moreover, there is a prefential localization of γδ T-cells expressing given Vgamma and Vdelta genes in certain tissues. In humans, γδ T-cells expressing the Vg9Vd2-encoded TCR account for anywhere between 50 and >95% of peripheral blood γδ T-cells, whereas cells expressing non-Vd2 genes dominate in mucosal tissues. In mice, there is an ordered appearance of γδ T-cell „waves“ during embryonic development, resulting in preferential localization of γδ T-cells expressing distinct VgammaVdelta genes in the skin, the reproductive organs, or gut epithelia. The major function of γδ T-cells resides in local immunosurveillance and immune defense against infection and malignancy. This is supported by the identification of ligands that are selectively recognized by the γδ TCR. As an example, human Vgamma9Vdelta2 T-cells recognize phosphorylated metabolites („phosphoantigens“) that are secreted by many pathogens but can also be overproduced by tumor cells, providing a basis for a role of these γδ T-cells in both anti-infective and anti-tumor immunity. Similarly, the recognition of endothelial protein C receptor by human non-Vdelta2 γδ T-cells has recently been identified to provide a link for the role for such γδ T-cells in immunity against epithelial tumor cells and cytomegalovirus-infected endothelial cells. In addition to „classical“ functions such as cytokine production and cytotoxicity, recent studies suggest that subsets of γδ T-cells can exert additional functions such as regulatory activity and – quite surpisingly – „professional“ antigen-presenting capacity. It is currently not well known how this tremendous extent of functional plasticity is regulated and what is the extent of γδ TCR ligand diversity. Due to their non-MHC-restricted recognition of unusual stress-associated ligands, γδ T-cells have raised great interest as to their potential translational application in cell-based immunotherapy. Topics of this Research Focus include: Molecular insights into the activation and differentiation requirements of γδ T-cells, role of pyrophosphates and butyrophilin molecules for the activation of human γδ T-cells, role of γδ T-cells in tumor immunity and in other infectious and non-infectious diseases, and many others. We are most grateful to all colleagues who agreed to write a manuscript. Thanks to their contributions, this E-book presents an up-to-date overview on many facets of the still exciting γδ T-cells.

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