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Allorecognition by Leukocytes of the Adaptive Immune System

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453863 Year: Pages: 107 DOI: 10.3389/978-2-88945-386-3 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2018-11-16 17:17:57
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The term allorecognition refers to the series of mechanisms used by an individual’s immune system to distinguish its own cells and tissues from those of another individual belonging to the same species. During evolution, different cells and molecules of both innate and adaptive immune systems have been selected to recognize and respond to antigens expressed by allogeneic cells, but not autologous cells (alloantigens). This research topic focuses on allorecognition by lymphocytes of the adaptive immune system and its involvement in rejection or tolerance of allogeneic transplants. T and B cells recognizing alloantigens via specific receptors become activated and undergo proliferation and differentiation into different types of effector and memory cells. Allorecognition by lymphocytes occurs regularly during pregnancy upon trafficking of both maternal and fetal cells. In this setting, allorecognition triggers an alloresponse that is protective towards the fetus thus preventing abortion. Protective alloimmunity is mediated through cooperation between different lymphocytes and antigen presenting cells (APCs), as well as regulatory mediators and receptors. Likewise, certain transplants placed in organs and tissues called immune-privileged sites such as the eye, the central nervous system and the testis elicit protective rather than destructive adaptive immune responses. Therefore, under certain circumstances, allorecognition by regulatory lymphocytes (Tregs and Bregs) can lead to tolerance of alloantigens. In contrast, allorecognition by T cells in non-immune privileged sites and under inflammatory conditions leads to a destructive immune response. Indeed, after transplantation of most allogeneic organs and tissues, activation of pro-inflammatory T cells (TH1 and TH17), which recognize donor MHC proteins (direct pathway) or peptides derived from donor MHC and minor antigens (indirect pathway), leads to graft rejection. This inflammatory response leads to the differentiation of allospecific cytotoxic T cells as well as production of donor specific antibodies by B cells, both of which contribute to the destruction of the transplant. In this Research Topic, we describe the different pathways of allorecognition by T cells involved in allograft rejection, as well as the role of different antigen presenting cells and graft-derived microvesicles (exosomes) involved in this process. Another aspect of this Research Topic addresses the essential role of alloreactive memory T cells in allograft rejection and resistance to transplant tolerance induction in laboratory rodents, as well as non-human primates and patients. Indeed, it has become evident that laboratory mice display very few memory alloreactive T cells pre-transplantation, essentially due to the fact that they are raised in pathogen-free facilities. In contrast, primates display high frequencies of alloreactive memory T cells, either generated through prior exposure to allogeneic MHC molecules or via cross-reactivity with microbial antigens. We and others have provided ample evidence showing that this feature accounts for differences in terms of tolerance susceptibility between laboratory rodents and patients. This implies that further investigation of tolerance protocols in laboratory mice should be performed using “dirty mice” i.e., mice raised in non-sterile conditions. In summary, this Research Topic addresses key aspects of allorecognition by lymphocytes and alloantigen presentation by dendritic cells, and specifically how these processes shape our immune system and govern the rejection or tolerance of allogeneic tissues and organs.

Animal allergens: Common protein characteristics featuring their allergenicity

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196203 Year: Pages: 88 DOI: 10.3389/978-2-88919-620-3 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2016-08-16 10:34:25
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Among the many molecules present in our environment, some have the property to induce allergic sensitization and IgE-mediated reactions. The analysis of known major animal allergens has shown that most belong to single protein families: lipocalins and serum albumins for inhalant allergens, EF-hand proteins, tropomyosins and caseins for the digestive allergens. The finding that allergens are often clustered in large families may be related to the fact that common structural, biochemical or functional features contribute to their allergenicity, in addition to external adjuvant factors. Currently, there is no curative treatment for animal allergy available. In order to lower allergic reactions to respiratory allergens in daily life and to food allergens upon accidental exposure, it is important to desensitize concerned patients. Tolerance induction by allergen-specific immunotherapy is in the current focus of an ambitious research. This Research Topic aims to provide a comprehensive view of the basic and recent insights on the allergenicity of animal allergens in view of their structural and functional aspects as well as allergen-specific immunotherapy.

Antibody Fc Engineering: Towards Better Therapeutics

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456789 Year: Pages: 118 DOI: 10.3389/978-2-88945-678-9 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2019-01-23 14:53:43
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Monoclonal antibodies and Fc-fusion proteins used clinically are Fc-based therapeutics that grow fastest in the pharmaceutical industry. Since they both contain an Fc fragment, engineering of Fc fragments could be a platform for improving Fc-based drug efficacy. Fc engineering includes various aspects: stabilization of Fc; regulation of effector functions including antibody-dependent cell-mediated cytotoxicity, complement-dependent cytotoxicity; extension of serum half-life by modification of neonatal Fc receptor (FcRn) binding; monomerization or heterodimerization of Fc for design of new Fc formats. Currently, many new methods are being used in Fc engineering. Compared to traditional methods such as site mutagenesis on certain positions by amino acid replacement, new methods such as display-based technology can confer high throughput screening and obtain optimized variants relatively quickly, accelerating the drug development process. With the new methods, many new Fc variants were identified. On this Research Topic we are going to review the progress in current Fc engineering including the new engineering methods and the Fc variants or constructs they have produced, and the potential of these new Fcs in clinical use.

Antibody Repertoire and Graft Outcome Following Solid Organ Transplantation

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452415 Year: Pages: 176 DOI: 10.3389/978-2-88945-241-5 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2017-10-13 14:57:01
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The first real major breakthrough that laid the basis of HLA antibody detection in the field of solid organ transplantation, came with the introduction of the complement dependent cytotoxicity (CDC) test in 1964 by Terasaki and McClelland. Since then, methods for antibody detection have evolved remarkably from conventional cell-based assays to the current advanced solid phase systems on the Luminex platform, with increasing degree of sensitivity and specificity. The latter have been indispensable for more accurate identification of donor specific HLA antibodies in broadly reactive allo antisera, and to guide donor selection and kidney paired exchange programs through virtual crossmatching, in addition to serving as excellent tools for initiating pre-transplant desensitization and post- transplant antibody monitoring. Consensus is evolving on the optimal routine employment of these methods in donor selection strategies along with an understanding of the clinical relevance of antibodies detected by each of them. The immunoassays based on the Luminex platform and flow cytometric beads are however unable to discriminate complement fixing from non-complement fixing HLA antibodies. This is important because the former are considered clinically more pertinent in the peri-transplant period. The C1q assay which is a modification of the solid phase assay based on Luminex single antigen beads, which can be used effectively to monitor high dose IVIG desensitization is essentially a surrogate complement fixing assay, retaining the exquisite sensitivity and specificity of the Luminex platform. Currently, information obtained from these assays is preliminary and much needs to be done to standardize technologies and set a consensus ‘MFI cut off’ for antibody positivity. Besides the overriding influence of anti-HLA antibodies on overall solid organ graft survival, immune response to non-HLA antigens has become a topic of substantial interest in recent years. An ever expanding list of non-HLA antigens has been implicated in graft rejection for various organs, of which the most noted are the Major Histocompatibility Complex class I chain-related molecule A (MICA), Vimentin, Myosin, Angiotensin II type 1 receptor (AT1R), Tubulin and Collagen. MICA is one of the most polymorphic and extensively studied non-HLA antigenic targets especially in renal transplantation. Although there are clear indications of MICA antibodies being associated with adverse graft outcome, to date a definitive consensus on this relationship has not been agreed. Because MICA molecules are not expressed constitutively on immunocompetent cells such as T and B lymphocytes, it is of utmost importance to address the impact of MICA donor specific antibodies (DSA) as compared to those that are non- donor specific (NDSA) on graft outcome. The soluble isoform of MICA molecule (sMICA) that is derived from the proteolytic shedding of membrane bound molecules has the potential to engage the NK-cell activating receptor NKG2D and down-regulate its expression. Consequent to the interaction of NKG2D by sMICA, the receptor ligand complex is endocytosed and degraded and thus suppresses NKG2D mediated lysis of the target by NK cells. Thus interaction between NKG2D and sMICA leads to expansion of immunosuppressive/anergic T cells thereby resulting in suppression of NKG2D mediated host innate immunity. These concept support the possible involvement of an immunosuppressive role for sMICA during allotransplantation as shown recently for heart transplantation. This research topic focuses on the clinical utility of investigating the complete antibody repertoire in solid organ transplantation.

Antimicrobial peptides and Complement - Maximising the inflammatory response

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197378 Year: Pages: 157 DOI: 10.3389/978-2-88919-737-8 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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Antimicrobial peptides and complement are distinct components of the innate immune defence. While antimicrobial peptides, after cleavage of a preproprotein, have the ability to insert directly in non host membranes, complement requires a sequential enzymatic activation in the fluid phase in order to produce a transmembrane membrane attack complex. Its insertion is controlled by membrane bound regulators. Deficiencies are described for both effectors and relate to increased susceptibility of infection. In addition, however, antimicrobial peptides and complement each influence the activity of inflammatory cells as recent data in the respective research areas shows. This series of articles draws together for the entities of antimicrobial peptides and complement a balance of contributions in the areas of evolution, roles, functions and preclinical applications. By comparing and contrasting antimicrobial peptides and complement, greater cross-disciplinary appreciation will be derived for their individual and overlapping spectra of activity, circumstances of activation and their general ability to more completely inform the inflammatory and cellular response.

Apoptotic Cell Clearance in Health and Disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456888 Year: Pages: 294 DOI: 10.3389/978-2-88945-688-8 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2019-01-23 14:53:43
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Clearance of apoptotic cells is essential for proper development, homeostasis and termination of immune responses in multicellular organisms. Thus, cellular and molecular players taking part in the sequential events of this process are of great interest. Research in the last 20 years has indicated that specific ligands and receptors take part in the attraction of immune cells toward apoptotic targets and in the interactions between apoptotic cells and professional as well as non-professional phagocytes that engulf them. Moreover, phagocytosis of apoptotic cells (efferocytosis) leads to significant phenotypic changes in the engulfing cells suggesting that it is a major fate-determining event for phagocytes. Particularly, efferocytosis has an important impact on the inflammation-resolution axis as well as embryonic development and tissue morphogenesis. Deficiencies in these processes can result in health threats, such as autoimmunity, atherosclerosis, bone loss, obesity, infertility, neurodegeneration, fibrosis and cancer. This eBook brings together 24 original research and review manuscripts that cover various aspects of apoptotic cell removal during normal development and homeostasis as well as in tumorigenesis and regenerative processes following injury.

Application of Antigen Cross-Presentation Research into Patient Care

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889451913 Year: Pages: 124 DOI: 10.3389/978-2-88945-191-3 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2017-10-13 14:57:01
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The activation of adaptive immune responses requires the processing and presentation of protein antigens to lymphocytes. Especially dendritic cells are effective at display of antigen-derived peptides in the form of immunogenic peptide/MHC complexes to CD4 and CD8-positive T cells, and can stimulate even naive T cells to clonally expand. During the last 40 years, mechanisms that facilitate antigen processing and presentation were clarified, mostly from work in cell lines and mouse models. From mouse-based work, it is now clear that dendritic cells represent a collection of specialized cell subsets that are particularly well endowed to stimulate antigen transport to distinct tissue locations, to transfer antigens between cellular subsets or to trigger T cell responses. Dendritic cell subsets hold great promise for therapeutic application, for example as dendritic cell-based vaccines to bolster immune responses against viruses or malignant growths. Hurdles remain that preclude the efficient application of high quality pre-clinical research into standardized patient care. In this research topic, efforts in dendritic cell research and dendritic cell-based vaccines are discussed, from both pre-clinical and application points of view.

Arrest chemokines

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194308 Year: Pages: 108 DOI: 10.3389/978-2-88919-430-8 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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Arrest chemokines are a small group of chemokines that promote leukocyte arrest from rolling by triggering rapid integrin activation. Arrest chemokines have been described for neutrophils, monocytes, eosinophils, naïve lymphocytes and effector memory T cells. Most arrest chemokines are immobilized on the endothelial surface by binding to heparin sulfate proteoglycans. Whether soluble chemokines can promote integrin activation and arrest is controversial (Alon-Gerszten). Many aspects of the signaling pathway from the GPCR chemokine receptor to integrin activation are the subject of active investigation. Leukocyte adhesion deficiency III is a human disease in which chemokine-triggered integrin activation is defective because of a mutation in the cytoskeletal protein kindlin-3. About 10 different such mutations have been described. The defects seen in patients with LAD-III elucidate the importance of rapid integrin activation for host defense in humans. We welcome reports that help clarifying this crucial first step in the process of leukocyte transendothelial migration.

Autoimmuno-Anti-Tumour Immunity (AATI) - Understanding the Immune Responses against "Self" & "Altered-self"

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889451906 Year: Pages: 174 DOI: 10.3389/978-2-88945-190-6 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2017-10-13 14:57:01
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The brief description of tumours being “wounds that do not heal” by Dr Harold F. Dworak nearly three decades ago (N Engl J Med 1986) has provided not only a vivid illustration of neoplastic diseases in general but also, in retrospect conceptually, a plausible immunological definition of cancers. Based on our current understanding in the field, it could have even a multi-dimensional meaning attached with. This relates to several important issues which need to be addressed further, i.e. in terms of a close link between chronic inflammation and tumourigenesis widely observed; clinical and experimental evidence of immunity against tumours versus the highly immunosuppressive tumour microenvironment being associated; and their underlying immunological mechanisms, oncogenic basis, as well as the true causal relationship in question. Recent findings from studies into the pathogenesis of autoimmunity and, more importantly, the mechanisms which protect against it, have offered some new insights for our understanding in this direction. Chronic or persistent autoimmune-like inflammatory conditions are evidently associated with tumor development. The important question is about their true causal relationship. Chronic or persistent inflammation has been shown to contribute directly to tumour development by triggering neoplastic transformation and production of inflammatory mediators which could promote cancer cell survival, proliferation and invasion. On the other hand, tumours are mutated self-tissue cells to which the host immune system is largely tolerized otherwise. Although the mutations may give rise to the expression of tumour-specific antigens (TSA) or tumour-associated antigens (TAA), most of these TSAs/TAAs are found to be poor immunogens. The ongoing inflammatory conditions may therefore reflect a desperate attempt of the host immune system to mount anti-tumour responses, though ineffectively, being a consequence of the continuous yet largely futile triggering by those poorly immunogenic TSAs/TAAs. Furthermore, during autoimmune or overtly persistent immunological responses, many regulatory mechanisms are triggered in the host in attempts to limit the ongoing harmful inflammatory reactions. Such a negative feedback regulation is known to be crucial in preventing normal individuals from immune-mediated diseases. As a result of the negative feedback loop, however, an excessive production of anti-inflammatory or immunosuppressive molecules followed by the exhaustion of the immune effector cells may instead lower the ability of the host immune system to mount specific anti-tumor responses, allowing the escape of tumour or mutated cells from immunosurveillance. This may also help to explain why the most effective way to enhance host immunity against cancer is by targeting the negative arm of immune regulation. In this Frontiers Research Topic, we aim to gather current views from experts in these inherent overlapping fields of oncology, autoimmunity and tumour immunology, and to make them available to our potential readership who may be particularly interested in this cutting-edge area. By understanding how the immune system is normally regulated, why dysregulation of which may cause the immunological-oncological related diseases, we also encourage further discussions as to how the so-called "self-reactivity" (autoimmune responses) can be alternatively switched on and redirected, immunologically or molecularly, for effective cancer treatment.

Bacterial Exotoxins: How bacteria fight the immune system

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199914 Year: Pages: 190 DOI: 10.3389/978-2-88919-991-4 Language: English
Publisher: Frontiers Media SA
Subject: Microbiology --- Science (General) --- Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-01-19 14:05:46
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The goal of this research topic was to gather current knowledge on the interaction of bacterial exotoxins and effector proteins with the host immune system. The following 16 research and review articles in this special issue describe mechanisms of immune modification and evasion and provide an overview over the complexity of bacterial toxin interaction with different cells of the immune system.

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