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The prevalence of asthma, rhinitis, and food allergies has increased dramatically over the last few decades. This increase originally started in western countries, but is now also evident in many other regions of the world. Given the fact that the increase is so quick, the noted increase cannot be linked to a genetic effect, and many environmental factors have been identified that are associated with increased or reduced prevalence of allergies, like changing dietary habits, increased urbanization, pollution, exposure to microorganisms and LPS, and the farming environment and raw milk consumption. Although the key role of allergen-specific IgE in allergies is well known, the role of allergen-specific IgG and IgA antibodies is less well defined. This review will provide an overview of the functions of allergen-specific IgE in allergy, the role of allergen-specific antibodies (IgG (4) and IgA) in allergen immunotherapy (AIT), the possibility to use allergen-specific antibodies for treatment of ongoing allergies, and the potential role of allergen-specific antibodies in tolerance induction to allergens in a preventive setting. In the last, more speculative, section we will present novel hypotheses on the potential role of allergen-specific non-IgE antibodies in allergies by directing antigen presentation, Th2 development, and innate immune training.

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Background: Allergens from Fagales trees frequently cause spring allergy in Europe, North America, and some parts of Asia. The definition of the birch homologous group, which includes birch (Bet v), oak (Que a), alder (Aln g), hazel (Cor a), hornbeam (Car b), beech (Fag s), and chestnut (Cas s), is based on high allergen sequence identity and extensive IgE cross-reactivity. Clinical effect was seen during the alder/hazel, birch, and oak pollen seasons after treatment with tree SLIT-tablets containing only birch allergen extract. Here, we characterize T-cell reactivity with respect to epitope specificities and cross-reactivity toward various Bet v 1 family members, (PR-10/group 1 major allergens). This cross-reactivity may be part of the immunological basis of clinical effect or cross-protection when exposed to birch homologous tree species. Method: T-cell lines were generated from 29 birch-allergic individuals through stimulation of peripheral blood mononuclear cells (PBMCs) with birch/Bet v or oak/Que a allergen extracts. T-cell responses to allergen extracts, purified group 1 allergens, and overlapping 20-mer peptides (Bet v 1, Aln g 1, Cor a 1, and Que a 1) were investigated by T-cell proliferation and cytokine production. Cross-reactivity was evaluated based on Pearson's correlations of response strength and further investigated by flow cytometry using tetramer staining for homologous peptide pairs. Results: T-cell reactivity toward extracts and group 1 allergens from across the birch homologous group was observed for birch/Bet v as well as oak/Que a T-cell lines. T-cell lines responded to multiple Bet v 1 homologous peptides from Aln g 1 and Cor a 1 and a subset of Que a 1 peptides. Significant Pearson's correlations between frequently recognized peptides derived from Bet v 1 and the corresponding peptides derived from alder, hazel, and oak strongly supported the T-cell cross-reactivity toward these allergens. Cross-reactivity between birch and birch homologous peptides was confirmed by pMHCII tetramer staining. Conclusion: T cells from birch tree pollen allergic individuals respond to multiple trees within the birch homologous group in accordance with the level of sequence homology between Bet v 1 family members, (PR-10 allergens) from these allergen sources, confirming the basis for clinical cross-protection.

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Both periodontitis and Coronavirus disease 2019 (COVID-19) pose grave threats to public health and social order, endanger human life, and place a significant financial strain on the global healthcare system. Since the COVID-19 pandemic, mounting research has revealed a link between COVID-19 and periodontitis. It is critical to comprehend the immunological mechanisms of the two illnesses as well as their immunological interaction. Much evidence showed that there are many similar inflammatory pathways between periodontitis and COVID-19, such as NF-κB pathway, NLRP3/IL-1ß pathway, and IL-6 signaling pathway. Common risk factors such as gender, lifestyle, and comorbidities contribute to the severity of both diseases. Revealing the internal relationship between the two diseases is conducive to the treatment of the two diseases in an emergency period. It is also critical to maintain good oral hygiene and a positive attitude during treatment. This review covers four main areas: immunological mechanisms, common risk factors, evidence of the association between the two diseases, and possible interventions and potential targets. These will provide potential ideas for drug development and clinical treatment of the two diseases.

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Melanocyte damage, innate immune response, adaptive immune response, and immune inflammatory microenvironment disorders are involved in the development of the immunological pathogenic mechanism of vitiligo. Mesenchymal stem cells are considered an ideal type of cells for the treatment of vitiligo owing to their low immunogenicity, lower rates of transplant rejection, and ability to secrete numerous growth factors, exosomes, and cytokines in vivo. The regulation of signaling pathways related to oxidative stress and immune imbalance in the immunological pathogenesis of vitiligo can improve the immune microenvironment of tissue injury sites. In addition, co-transplantation with melanocytes can reverse the progression of vitiligo. Therefore, continuous in-depth research on the immunopathogenic mechanism involved in this disease and mesenchymal stem cell-based therapy is warranted for the treatment of vitiligo in the future.

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Vaccines are one of the most successful medical inventions to enable the eradication or control of common and fatal diseases. Environmental exposure of hosts, including helminth infections, plays an important role in immune responses to vaccines. Given that helminth infections are among the most common infectious diseases in the world, evaluating vaccine efficiency in helminth-infected populations may provide critical information for selecting optimal vaccination programs. Here, we reviewed the effects of helminth infections on vaccination and its underlying immunological mechanisms, based on findings from human studies and animal models. Moreover, the potential influence of helminth infections on SARS-CoV-2 vaccine was also discussed. Based on these findings, there is an urgent need for anthelmintic treatments to eliminate helminth suppressive impacts on vaccination effectiveness during implementing mass vaccination in parasite endemic areas.

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mRNA therapy is a novel anticancer strategy based on in vitro transcription (IVT), which has potential for the treatment of malignant tumors. The outbreak of the COVID-19 pandemic in the early 21st century has promoted the application of mRNA technologies in SARS-CoV-2 vaccines, and there has been a great deal of interest in the research and development of mRNA cancer vaccines. There has been progress in a number of key technologies, including mRNA production strategies, delivery systems, antitumor immune strategies, etc. These technologies have accelerated the progress and clinical applications of mRNA therapy, overcoming problems encountered in the past, such as instability, inefficient delivery, and weak immunogenicity of mRNA vaccines. This review provides a detailed overview of the production, delivery systems, immunological mechanisms, and antitumor immune response strategies for mRNA cancer vaccines. We list some mRNA cancer vaccines that are candidates for cancer treatment and discuss clinical trials in the field of tumor immunotherapy. In addition, we discuss the immunological mechanism of action by which mRNA vaccines destroy tumors as well as challenges and prospects for the future.

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Intense mental stimulation and stress often directly induce or exacerbate psoriasis. On the contrary, patients with nerve injury and nervous system dysfunction have psoriasis remission. The nervous system plays an important role in the inflammatory process of psoriasis, and neuropeptides are considered as local mediators of disease maintenance. To examine the molecular mechanism involved in this, first we analyzed calcitonin gene-related peptide (CGRP)-treated langerhans Cells and γδ-T cells separately. CGRP induced IL-23 mRNA and protein expression via PDK1-Rsk signaling pathway. However, CGRP had no effect on secretion of IL-17A and IL-22 in γδ-T cells. Then we treated LCs/γδ-T cells Co-culture Model with CGRP. CGRP upregulated IL-17A and IL-22 expression in co-culture model through the paracrine effect of LCs. IL-17A and IL-22 are key cytokines of psoriasis. These findings provide a potential mechanism by which nerve factors affect the development of psoriasis.

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COVID-19 deteriorates type II pneumocytes and damages the alveolar immunologic balancing process through the inadvertent activation of a sequence of localized and general inflammatory responses. Due to an aggregation of uncleaved angiotensin II, the stimulated inflammatory cells cause cytokines synthesis and secretion (cytokine storming). The cytokines cause the systemic inflammatory response syndrome (SIRS), leading to widespread tissue injuries. Consequently, pro-coagulant factors are activated which increases the microthrombi in different tissues, resulting in ischemia, multiple organ dysfunction syndrome, acute respiratory distress syndrome, and increased mortality. Vaccines recipients (via virus vector technology) have reported the incidence of thrombocytopenia and peculiar thrombotic events. After vaccination, using sera from patients who experienced thrombocytopenia and thrombosis showed increased reactivity in anti-PF4/heparin enzyme immunoassays and substantial platelet-activating antibodies (positive). In some sera of individuals suffering from heparin-induced thrombocytopenia (HIT), it has been observed that platelet-activating antibodies resulting from vaccination tend to bind to non-complexed PF4 alone.

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@#Oral lichen planus (OLP) is a common chronic disease of the oral mucosa with unclear pathogenesis. Local infiltration of T cells plays a key role in the pathological process of OLP. Increased evidence supports the notion that the imbalance of helper T cells (Th) 1/Th2 and Th17/regulatory T cells (Treg) and their related cytokines is closely related to the pathogenesis and progression of OLP. In recent years, studies have shown that OX40 (CD134) and its ligand OX40L (CD252) play an important role in the process of the T-cell immune response. They participate in the balance regulation of Th1/Th2 and Th17/Treg, mediate the imbalance of pro-inflammatory and anti-inflammatory, and affect the occurrence and development of a variety of autoimmune diseases. However, there is no direct evidence that the OX40/OX40L axis mediates the imbalance of T-cell subsets in the pathogenesis of OLP. Therefore, large sample clinical as well as in vitro and in vivo experimental studies on the mechanism by which the OX40/OX40L axis regulates the balance of T-cell subsets in OLP are still needed in the future.

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The amyloid plaques (Aβ) hypotheses and Tau propagation hypothesis are still proposed as the most prevailing causes for Alzheimer's disease (AD). Recent compelling evidences have firmly demonstrated that there are tight involvements of dysfunction of the immune system in the pathogenesis and progression of AD. Here, we review the current knowledge on the role of immune system in pathogenesis of AD and discuss the most relevant findings in immunotherapies for AD to help clinician to further consider the possible direction of diagnosis and treatment of AD.

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A scar is a local symptom, which results from severe physical, biological and chemical damage to human skin and soft tissue. Scars can affect both skin appearance and function. The affected skin or soft tissue cannot be completely repaired normally by itself and is replaced by formed fibrous tissue. Patients with scars can develop physical pain and mental conditions, especially those with scars left after burns, scalds and severe traumas. The scar proliferation phase can be up to several years which could be almost unbearable for patients. Also, the atrophic period afterwards makes the patient's face unrecognizable and dysfunctional, causing great physical and mental impairment. Therefore, scar repair is of great clinical importance for patients, and understanding the immunological mechanisms of scar repair is an important prerequisite for the effective treatment of scars. This study is a systematic review of current research advances about the immunological mechanisms of scar repair, so as to provide a reference for the selection of regimens in clinical treatment.

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Evolving data show a variable expression of clinical neurological manifestations in patients suffering with coronavirus disease 2019 (COVID-19) from early disease onset. The most frequent symptoms and signs are fatigue, dizziness, impaired consciousness, ageusia, anosmia, radicular pain, and headache, as well as others. Based on the high number of series of cases reported, there is evidence for the implication of the immune system in the pathological mechanism of COVID-19. Although the exact role of the immunological mechanism is not elucidated, two main mechanisms are suggested which implicate the direct effect of severe acute respiratory syndrome coronavirus 2 infection in the central nervous system and neuroinflammation. In the context of neurological manifestations associated with COVID-19, neuropsychiatric disorders show an exacerbation and are described by symptoms and signs such as depression, anxiety, mood alterations, psychosis, post-traumatic stress disorder, delirium, and cognitive impairment, which appear to be common in COVID-19 survivors. A worsened score on psychopathological measures is seen in those with a history of psychiatric comorbidities. We review the neuropsychiatric manifestations associated with COVID-19 and some critical aspects of the innate and adaptive immune system involved in mental health disorders occurring in COVID-19.

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BACKGROUND: The host innate immune system can recognize Pathogen-Associated Molecular Patterns (PAMPs) through Pattern Recognition Receptors (PRRs), thereby initiating innate immune responses and subsequent adaptive immune responses. PAMPs can be developed as a vaccine adjuvant for modulating and optimizing antigen-specific immune responses, especially in combating viral infections and tumor therapy. Although several PAMP adjuvants have been successfully developed they are still lacking in general, and many of them are in the preclinical exploration stage. OBJECTIVE: This review summarizes the research progress and development direction of PAMP adjuvants, focusing on their immune mechanisms and clinical applications. METHODS: PubMed, Scopus, and Google Scholar were screened for this information. We highlight the immune mechanisms and clinical applications of PAMP adjuvants. RESULTS: Because of the differences in receptor positions, specific immune cells targets, and signaling pathways, the detailed molecular mechanism and pharmacokinetic properties of one agonist cannot be fully generalized to another agonist, and each PAMP should be studied separately. In addition, combination therapy and effective integration of different adjuvants can increase the additional efficacy of innate and adaptive immune responses. CONCLUSION: The mechanisms by which PAMPs exert adjuvant functions are diverse. With continuous discovery in the future, constant adjustments should be made to build new understandings. At present, the goal of therapeutic vaccination is to induce T cells that can specifically recognize and eliminate tumor cells and establish long-term immune memory. Following immune checkpoint modulation therapy, cancer treatment vaccines may be an option worthy of clinical testing.

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BACKGROUND: The SQ tree SLIT-tablet (containing birch extract) proved clinically significant effects during the pollen season for birch as well as alder/hazel. Immune outcomes of this treatment for allergens from multiple birch homologous trees need further investigation. We hypothesize that birch pollen extract AIT modulates a highly cross-reactive immune response and that this may be the basis for the observed clinical cross-protection. METHODS: Blood samples were collected from 397 birch allergic patients during SQ tree SLIT-tablet or placebo treatment (1:1) for up to 40 weeks. Serum IgE and IgG4 specific to birch, and birch homologous tree pollens from alder, hazel, hornbeam, beech and chestnut were measured by ImmunoCAP. IgE-Blocking Factor (IgE-BF) for alder, birch and hazel during treatment was measured by Advia Centaur and blocking effects for birch and all these birch homologous tree pollens were further investigated by basophil activation (BAT). Antibody readouts were investigated in patient subsets. T-cell responses (proliferation) to allergen extracts and peptide pools (group 1 allergens) were investigated in T-cell lines from 29 untreated birch pollen-allergic individuals. RESULTS: Significant Pearson correlations between serum IgE towards birch, alder, hazel, hornbeam and beech were observed (r-values > .86). T-cell reactivity was observed throughout the birch homologous group. Almost identical kinetics for changes in IgE towards birch, alder and hazel were observed during treatment and similar species-specific changes were seen for serum-IgG4 . IgG4 reactivity towards birch and alder, hazel, hornbeam and beech correlated significantly at end-of-treatment (r-values > .72). Treatment resulted in similar IgE-BF kinetics for alder, birch, and hazel and blocking of BAT for multiple trees in most actively treated patients investigated. CONCLUSIONS: Systematic analyses of T-cell and antibody cross-reactivities before and during birch pollen extract AIT provide the immunological basis for the observed clinical effect of SQ tree SLIT-tablet treatment of tree pollen allergy induced by multiple trees in the birch homologous group.

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Vaccines are considered one of the most important bioproducts in medicine. Since the development of the smallpox vaccine in 1796, several types of vaccines for many diseases have been created. However, some vaccines have shown limitations as high cost and low immune responses. In that regard, bacteriophages have been proposed as an attractive alternative for the development of more cost-effective vaccines. Phage-displayed vaccines consists in the expression of antigens on the phage surface. This approach takes advantage of inherent properties of these particles such as their adjuvant capacity, economic production and high stability, among others. To date, three types of phage-based vaccines have been developed: phage-displayed, phage DNA and hybrid phage-DNA vaccines. Typically, phage display technology has been used for the identification of new and protective epitopes, mimotopes and antigens. In this context, phage particles represent a versatile, effective and promising alternative for the development of more effective vaccine delivery systems which should be highly exploited in the future. This review describes current advances in the development of bacteriophage-based vaccines, with special attention to vaccine delivery strategies. Moreover, the immunological aspects of phage-based vaccines, as well as the applications of phage display for vaccine development, are explored. Finally, important challenges and the future of phage-bases vaccines are discussed.

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Amyotrophic lateral sclerosis (ALS) is a disease of which the underlying etiology and pathogenesis are unknown. Numerous data indicate an important role of the immune system and mitochondrial function in the disease. Primary biliary cirrhosis (PBC) is an autoimmune liver disease resulting from a combination of genetic and environmental risk factors. Patients with PBC develop innate and adaptive immune reactions against mitochondrial antigens. Therefore, common mechanisms could exist in both diseases. We present two cases of ALS with PBC to explore the relationship between the two diseases from the immunological and mitochondrial aspects. Further attention should be given to immune-modulating therapy in ALS patients.

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Mycoplasma pneumoniae pneumonia (MPP) is caused by Mycoplasma pneumoniae infection with respiratory tract infection with pneumonia.Recently,the incidence of MPP has been increasing year by year,and the age of onset has an earlier trend.It is easy to recur after the infection of Mycoplasma pneumoniae (MP).The MP not only can cause respiratory disease,but also cause a wide range of extrapulmonary manifestations.Part of patients have rapid progression of disease and severe illness.Nowadays,the pathogenesis of MPP is not yet completely clear.It may be related to the direct adhesion and invasion of MP in the respiratory epithelium,toxic injury,and immunological mechanism.At present,a large number of studies have confirmed that the immune disorder and immune imbalance play a vital role in the development of MPP.This article reviews the latest research on the immunological mechanisms associated with Mycoplasma pneumonia.

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Ultraviolet light hardening therapy is an effective method for the treatment of polymorphic light eruption (PLE) . Recent studies have shown that narrow-band ultraviolet B (NB-UVB) is effective and safe for the prevention of recurrence of PLE. However, its treatment mechanisms still need further elucidation, and clinical studies with large sample size are needed for long-term tracking and assessment of initial dose of photohardening, dose-addition principle, treatment frequency and maintenance treatment protocols, in order to confirm the clinical application value of ultraviolet light photohardening therapy.