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Immunoglobulin E (IgE) plays a critical role for the immune system, fighting against parasites, toxins, and cancer. However, when it reacts to allergens without proper regulation, it can cause allergic reactions, including anaphylaxis, through a process initiated by effector cells such as basophils and mast cells. These cells display IgE on their surface, bound to the high-affinity IgE receptor FcεRI. A cross-linking antigen then triggers degranulation and the release of inflammatory mediators from the cells. Therapeutic monoclonal anti-IgE antibodies such as omalizumab, disrupt this process and are used to manage IgE-related conditions such as severe allergic asthma and chronic spontaneous urticaria. Interestingly, naturally occurring anti-IgE autoantibodies circulate at surprisingly high levels in healthy humans and mice and may thus be instrumental in regulating IgE activity. Although many open questions remain, recent studies have shed new light on their role as IgE regulators and their mechanism of action. Here, we summarize the latest insights on natural anti-IgE autoantibodies, and we compare their functional features to therapeutic monoclonal anti-IgE autoantibodies. [ABSTRACT FROM AUTHOR]

The article discusses the presence of mouse IgG antibodies in the widely used mouse IgE clone SPE-7, which is used to study IgE biology and function. The study found that SPE-7 contains IgG2a/b-IgE complexes, which can alter the functional profile of IgE. The presence of IgG in SPE-7 was confirmed through various assays, including enzyme-linked immunosorbent assays (ELISA) and liquid chromatography-mass spectrometry (LC-MS). These findings challenge the concept that IgE exerts antigen-independent effects on mast cell degranulation and survival. The study suggests that the presence of contaminating IgGs in therapeutic IgE antibodies should be considered, as they may alter the functional and pharmacological profile of these antibodies. [Extracted from the article]

The rising global incidence of IgE-mediated allergic reactions poses a significant challenge to the quality of life of affected individuals and to healthcare systems, with current treatments being limited in effectiveness, safety, and disease-modifying capabilities. IgE acts by sensitizing the highaffinity IgE receptor FcεRI expressed by mast cells and basophils, tuning these cells for inflammatory degranulation in response to future allergen encounters. In recent years, IgG has emerged as an essential negative regulator of IgE-dependent allergic inflammation. Mechanistically, studies have proposed different pathways by which IgG can interfere with the activation of IgE-mediated inflammation. Here, we briefly summarize the major proposed mechanisms of action by which IgG controls the IgE-FceRI inflammatory axis and how those mechanisms are currently applied as therapeutic interventions for IgE-mediated inflammation. [ABSTRACT FROM AUTHOR]

Introduction: Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury (ALI) resulting in life‐threatening hypoxaemia. Although ARDS can be caused by a variety of pathogens or major trauma, it is best known as the major cause of mortality in COVID‐19 patients. Since ARDS is often associated with dysregulated inflammatory immune responses, immunomodulatory approaches represent a possible treatment option. The objective of this study was to evaluate the therapeutic potential of interleukin (IL)‐1 blockade using Anakinra in a mouse model of lipopolysaccharide (LPS)‐induced ALI. Methods: We evaluated the effects of a daily subcutaneous Anakinra treatment in a mouse model of LPS‐induced ALI. We monitored body weight to assess the general health status of the mice. Two days after ALI induction, we evaluated the inflammatory cytokine MIP‐2 as well as protein levels in bronchoalveolar lavage (BAL) fluids. Two and nine days after ALI induction, we evaluated infiltrating leukocytes in BAL fluid and lung tissue. Results: Anakinra treatment reduced ALI‐induced weight loss compared to nontreated groups. At Day 2, Anakinra treatment reduced levels of MIP‐2 and protein in BAL fluids and reduced frequencies of NK cells and neutrophils in the lung tissue. Nine days after ALI induction, Anakinra treated mice displayed reduced levels of neutrophils and alveolar macrophages in BAL fluids. Conclusions: IL‐1 blockade using Anakinra reduced classical hallmarks of inflammation in a mouse model of ALI. Our data support ongoing and future research on the evaluation of Anakinra as a potential treatment option in ARDS. [ABSTRACT FROM AUTHOR]

Virus-like particles (VLPs) and nano-particles (NPs) are promising vaccine platforms that have led to the successful development of commercially available vaccines. The 5th international virus-like particle and nano-particle vaccines conference was held in Bern, Switzerland, from the 25th to the 27th of September in 2018. Topics included novel vaccine production techniques, methods to enhance vaccine immunogenicity, and preclinical/clinical efficacy evaluation of vaccine candidates. Here, we report on a selection of updates that were presented including the production of vaccines in plants, novel adjuvants to enhance vaccine immunogenicity, novel techniques of conjugating vaccine platforms with target antigens and the use of VLP-based vaccines for cancer and inflammatory diseases. [ABSTRACT FROM AUTHOR]