Clinical Reviews in Allergy & Immunology最新文献

The skin surface hosts diverse skin microbiota, including bacteria, fungi, and viruses. Intricate interactions between the skin microenvironment and microbial community are crucial for maintaining cutaneous homeostasis. This review explores the bidirectional relationship between the skin ecosystem and its microbiota. The skin microenvironment is shaped by a combination of intrinsic factors, dominated by sweat glands and pilosebaceous units, and external factors, such as UV radiation and personal care products, which create distinct niches that influence microbial colonization patterns across different skin regions. The skin microbiome, in turn, modulates the physical, chemical, immunological, and microbial barriers of the skin. We also discuss the alterations in this crosstalk in various immune-related skin conditions such as atopic dermatitis, psoriasis, rosacea, hidradenitis suppurativa, skin cancer, and aging. Understanding these interactions is vital for developing targeted microbiome-based therapies for various skin disorders. Further researches are needed to deepen insights into the microbial roles and their therapeutic potentials in skin health and disease.

Allergic reactions in dental practice have been a serious problem, causing various clinical symptoms and having a significant impact on the quality of dental care. This study examined various aspects of allergic reactions, their causes, mechanisms of development, and prevalence in dental practice. The purpose of the study was to conduct a comprehensive analysis of allergic reactions, their classification, clinical manifestations, and mechanisms of development, and to identify the most common causes of such reactions. To achieve this goal, a systematic literature review was conducted. As a result of the study, different types of allergic reactions and mechanisms of their development were identified. Among them, special attention was paid to immediate hypersensitivity reactions mediated by immunoglobulin E (IgE). Delayed-type reactions mediated by sensitised T lymphocytes were also considered. Pseudoallergic reactions occupied a separate place in the classification of allergic reactions. The study emphasised the importance of cross-reactions, in which several structurally similar molecules bind to the same IgE antibodies or T lymphocytes. The main results of the study showed that allergic reactions can be triggered by a variety of allergens. Prominent among these were local anaesthetics such as lidocaine and benzocaine, antibiotics including penicillins and cephalosporins, latex products such as gloves and cofferdams, acrylic materials used in dental prostheses and fillings, and metal alloys containing nickel, chromium, and cobalt. The study has contributed to a better understanding of the factors causing allergic reactions in dental practice and the mechanisms of their development. This is important for improving the diagnosis and management of such cases, thereby improving the quality of dental care provided.

Sjögren's syndrome (SS) is a chronic autoimmune disorder that primarily affects the exocrine glands. Due to the intricate nature of the disease progression, the exact mechanisms underlying SS are not completely understood. Recent research has highlighted the complex interplay between immune dysregulation and metabolic abnormalities in inflammatory diseases. Notably, lipid metabolism has emerged as a crucial factor in the modulation of immune function and the progression of autoimmune diseases, including SS. This review explores the prevalence of dyslipidemia in SS, emphasizing its role in the onset, progression, and prognosis of the disease. We specifically described the impact of altered lipid metabolism in exocrine glands and its association with disease-specific features, including inflammation and glandular dysfunction. Additionally, we discussed the potential clinical implications of lipid metabolism regulation, including the role of polyunsaturated fatty acids (PUFAs) and their deficits in SS pathogenesis. By identifying lipid metabolism as a promising therapeutic target, this review highlights the need for further research into lipid-based interventions for the management of SS.

Autoimmune diseases are characterized by the dysregulation of B-cells, which are responsible for antibody production against pathogens, and T-cells, which play a crucial role in cell-mediated immunity, including both helper and cytotoxic T-cells. These disorders frequently present with abnormal responses from both B- and T-cells, which can have a significant impact on cardiovascular health, particularly among the female patients. Key mechanisms contributing to these diseases include the activation of the NLRP3 inflammasome impaired efferocytosis is the process by which phagocytes clear apoptotic cells to maintain immune and developmental balance. Defects in this process can lead to inflammatory and autoimmune disorders. The gut microbiota helps defend against pathogens and signals immune cells, playing a vital role in human health and is involved in many aspects of the body. Novel therapeutic strategies such as nanomedicine and targeted treatments are being developed to restore immune balance. The significance of thymic homeostasis the influence of viral infections and the presence of tertiary lymphoid structures highlight the need for multidisciplinary approaches in the management of these conditions. A case study of a 9-year-old girl diagnosed with seronegative autoimmune encephalitis, who displayed severe obsessive-compulsive disorder (OCD) and aggressive behavior, exemplifies the complexities involved in treatment. Promising interventions, including CAR-T-cell therapy and nanomedicine, are under development for various autoimmune diseases, such as vitiligo and refractory autoimmune rheumatic diseases (ARDs). Furthermore, emerging therapies, including CAR-T-cell therapy, mRNA-based strategies, and microbiome modulation, are being explored alongside advancements in personalized medicine and early diagnostic techniques to improve patient outcomes for individuals affected by autoimmune diseases.

Allergic and autoimmune disorders are characterised by dysregulation of the immune responses to otherwise inert environmental substances and autoantigens, leading to inflammation and tissue damage. Their incidence has constantly increased in the last decades, and their co-occurrence defies current standards in patient care. For years, allergy and autoimmunity have been considered opposite conditions, with IgE and Th2 lymphocytes cascade driving canonical allergic manifestations and Th1/Th17-related pathways accounting for autoimmunity. Conversely, growing evidence suggests that these conditions not only share some common inciting triggers but also are subtended by overlapping pathogenic pathways. Permissive genetic backgrounds, along with epithelial barrier damage and changes in the microbiome, are now appreciated as common risk factors for both allergy and autoimmunity. Eosinophils and mast cells, along with autoreactive IgE, are emerging players in triggering and sustaining autoimmunity, while pharmacological modulation of B cells and Th17 responses has provided novel clues to the pathophysiology of allergy. By combining clinical and therapeutic evidence with data from mechanistic studies, this review provides a state-of-the-art update on the complex interplay between allergy and autoimmunity, deconstructing old dichotomic paradigms and offering potential clues for future research.

Under the concept of "one airway, one disease", upper and lower airway inflammatory diseases share similar pathogenic mechanisms and are collectively referred to as airway inflammatory diseases. With industrial development and environmental changes, the incidence of these diseases has gradually increased. Traditional treatments, including glucocorticoids, antihistamines, and bronchodilators, have alleviated much of the discomfort experienced by patients. However, conventional drug delivery routes have inherent flaws, such as significant side effects, irritation of the respiratory mucosa, and issues related to drug deactivation. In recent years, nanomaterials have emerged as excellent carriers for drug delivery and are being increasingly utilized in the treatment of airway inflammatory diseases. These materials not only optimize the delivery of traditional medications but also facilitate the administration of various new drugs that target novel pathways, thereby enhancing the treatment outcomes of inflammatory diseases. This study reviews the latest research on nano-drug delivery systems used in the treatment of airway inflammatory diseases, covering traditional drugs, immunotherapy drugs, antimicrobial drugs, plant-derived drugs, and RNA drugs. The challenges involved in developing nano-delivery systems for these diseases are discussed, along with a future outlook. This review offers new insights that researchers can utilize to advance further research into the clinical application of nano-drug delivery systems for treating airway inflammatory diseases.

Atopic dermatitis (AD) is a chronic inflammatory skin disease with a complex relationship to allergens. While AD itself is not an allergic reaction and does not necessarily involve allergen sensitization, AD patients show higher rates of sensitization to food and inhalant allergens compared to the general population. Recent evidence refining the "dual allergen exposure hypothesis" demonstrates that early oral exposure to allergens through an intact gastrointestinal barrier typically promotes tolerance, while exposure through compromised skin or respiratory barriers often leads to sensitization. Therefore, the impaired skin barrier function in AD patients increases the risk of transcutaneous sensitization and may interfere with oral tolerance development. Interestingly, AD patients' sensitivity to contact allergens (such as metals and fragrances) is not necessarily higher than that of the general population, which may be related to the inherent properties of these allergens. Personalized allergen testing can help guide appropriate allergen avoidance and reintroduction strategies in AD management. The insights into optimal allergen exposure conditions have also expanded the potential applications of allergen-specific immunotherapy in preventing AD onset in high-risk populations and halting the atopic march.

Systemic lupus erythematosus (SLE) is an autoimmune disease that significantly increases the risk of cardiovascular diseases, particularly atherosclerosis (AS). Understanding the shared pathogenic mechanisms underlying SLE and AS is crucial for developing effective therapeutic strategies. Macrophages, as pivotal immune cells, play a critical role in the initiation and progression of atherosclerotic plaques within the context of SLE. This review delves into the molecular and cellular mechanisms governing macrophage activation and differentiation in response to SLE-related inflammatory mediators, highlighting their roles in lipid metabolism, plaque stability, and immune regulation. Additionally, we discussed the current treatment modalities for SLE and their impact on macrophage functionality, exploring these effects for atherosclerotic progression. By elucidating the intricate relationship between macrophages, SLE pathophysiology, and AS progression, this review underscores the need for a multidisciplinary approach in managing SLE and its cardiovascular complications, aiming to improve patient survival and quality of life through tailored therapeutic interventions addressing both autoimmune and cardiovascular pathologies.

Electronic cigarettes (EC) have emerged as a popular alternative to traditional tobacco products, but their impact on immune function has raised significant health concerns. This review explores the immunological effects of EC exposure, focusing on innate and adaptive immune responses. Electronic cigarette aerosol (ECA) induces widespread inflammation. These changes compromise immune cell function, impairing neutrophil chemotaxis, phagocytosis, and oxidative burst while increasing macrophage and dendritic cell recruitment and activation. ECA also disrupts epithelial barriers, increasing susceptibility to bacterial and viral infections. Studies show enhanced biofilm formation in bacteria such as Staphylococcus aureus and Streptococcus pneumoniae and impaired antiviral responses against pathogens like influenza A and SARS-CoV-2. Additionally, EC exposure modulates adaptive immunity, affecting T and B cell function and increasing systemic inflammatory markers. The long-term consequences of these immunological disruptions include heightened risks for chronic inflammatory diseases, respiratory infections, and potentially autoimmune conditions. The widespread adoption of EC, particularly among younger users, poses a growing public health challenge. As the popularity of vaping continues to rise, these immunological disruptions could result in increased healthcare burdens in the future, with higher rates of infections, chronic inflammatory diseases, and immune system-related disorders among those who begin using e-cigarettes at a young age. Understanding the full scope of EC-related health risks is essential for informing public health policies and protecting future generations from the potential long-term effects of vaping.

The intestinal microbiota is a complex community of organisms present in the human gastrointestinal tract, some of which can produce short-chain fatty acids (SCFAs) through the fermentation of dietary fiber. SCFAs play a major role in mediating the intestinal microbiota's regulation of host immunity and intestinal homeostasis. Respiratory syncytial virus (RSV) can cause an imbalance between anti-inflammatory and proinflammatory responses in the host. In addition, changes in SCFA levels and the structure of the intestinal microbiota have been observed after RSV infection. Therefore, there may be a link between SCFAs and RSV infection, and SCFAs are expected to be therapeutic targets for RSV infection.