Clinical Reviews in Allergy & Immunology最新文献

Background: The characteristics of Behçet's disease (BD) in individuals of Sub-Saharan ancestry (sub-SA) are poorly understood.

Methods: Herein, we conducted a PRISMA-compliant systematic review using the PubMed/Medline, Scopus, and Web of Science databases. Articles published up to September 1, 2023 were searched with the following keywords: "Behçet's disease" OR "Behcet's syndrome" AND "sub-Saharan African" OR "Black" OR "African". Data on the year, type and country of study, sample size, region of origin, nationality, age, sex, time to diagnosis, death, HLAB51 status, mucosal, and organ involvement were collected. Involvement of the central nervous system was retained on the basis of objective criteria, and dichotomized into parenchymal or non-parenchymal/vascular lesions. The pooled frequency of patients' main characteristics was calculated using a DerSimonian-Laird random-effects meta-analysis.

Results: This study included 42 full-text reports, with study periods ranging from 1970 to 2023. Overall, 230 adult patients (69% of males) were included, of whom 195 (85%) were from sub-Saharan African countries, 22 (10%) patients were from the Caribbean, and 13 (5%) patients were from the Americas, including 12 African Americans, and 1 African Brazilian. Oral and genital ulcers were reported in 98% [95% CI 91 to 100%] and 85% [72 to 92%], respectively. Ocular involvement occurred in 43% [31 to 56%] of patients. Central nervous system (CNS) involvement affected 39% [25 to 54] of the patients. Among them, 30% of patients had a cerebro-vascular disease, and 72% had a parenchymal involvement. The patients were mostly treated with oral steroids and colchicine, and remission was achieved in 35/54 (65%) patients, but 15 (69%) of them suffered severe sequelae, particularly ophthalmological and neurological.

Conclusion: Behçet's disease in patients of sub-Saharan ancestry appears to be predominantly HLA B51/B5-negative, and more severe than in other ethnicities, owing to a high prevalence of CNS involvement.

Inflammatory skin diseases and skin cancers are usually accompanied by metabolic comorbidities or altered metabolic status. Metabolomic analysis indicates that patients with inflammatory skin diseases and skin cancers exhibit altered metabolites, including glycans, lipids, and amino acids. This suggests that metabolic reprogramming may play a pivotal role in the pathogenesis of these skin diseases. The solute carrier (SLC) superfamily is responsible for the transport of a range of metabolites, which may serve as crucial intermediate links in the metabolic reprogramming of diseases. Nevertheless, research on the SLC superfamily in skin diseases remains limited, and the development of its drug targets is even more scarce. Therefore, this review is devoted to elucidating our current understanding of the role of the SLC family in the pathogenesis of inflammatory skin diseases and skin cancers, with a particular emphasis on its role in metabolic reprogramming. In doing so, we aim to provide a reference point for the subsequent development of drug targets for the SLC family in skin diseases.

Psoriasis is a chronic, immune-mediated inflammatory disorder marked by a complex interplay between genetic predisposition, cytokine dysregulation, and environmental triggers. Originally perceived as a superficial dermatological condition, it is now recognized as a systemic disease with far-reaching health implications. Advances in molecular genetics have uncovered over 80 susceptibility loci, with key variants such as HLA-C*06:02, IL23R, and CARD14 contributing to the multifactorial nature of the disorder. Central to its pathogenesis is the aberrant activation of the IL-23/Th17 axis, resulting in excessive production of proinflammatory cytokines that promote rapid keratinocyte proliferation and sustained inflammation. Epigenetic modifications further influence gene expression, while interactions with environmental factors, such as mechanical stress, ultraviolet exposure, and air pollution, exacerbate the inflammatory cascade. Recent progress in targeted therapeutic strategies, notably biologic agents and small molecule inhibitors, has transformed the treatment landscape by specifically modulating these pathogenic pathways. Such innovations are paving the way toward personalized medicine, aiming to optimize therapeutic outcomes and reduce the overall disease burden. This review offers a comprehensive synthesis of current knowledge on the genetic, immunologic, and molecular mechanisms underlying psoriasis. The review emphasizes recent advances in targeted therapies underlining the potential for translational applications that address both cutaneous manifestations and systemic inflammation. It also explores global disparities in psoriasis care and the need for inclusive approaches that bridge disparities and promote equitable, innovative disease management strategies.

Alterations in gut microbiota composition are increasingly recognized as key contributors to autoimmune disease pathogenesis. While dominant phyla such as Firmicutes and Bacteroidetes have been extensively studied at the phylum level, the immunomodulatory roles of specific members within these groups particularly the abundant but mechanistically underexplored Faecalibacterium prausnitzii (a member of Firmicutes) and Akkermansia muciniphila (of Verrucomicrobia) remain insufficiently characterized. In particular, current literature primarily focuses on associative findings, and integrated analyses elucidating disease-specific mechanisms and therapeutic relevance are still lacking. In this review, we synthesize mechanistic and disease-specific evidence regarding these two bacterial species across six autoimmune diseases, including systemic lupus erythematosus (SLE), type 1 diabetes (T1D), and rheumatoid arthritis (RA). F. prausnitzii is consistently depleted in autoimmune contexts and exerts protective effects through multiple mechanisms, including short-chain fatty acid (SCFA) production, histone deacetylase (HDAC) inhibition, Treg induction, secretion of microbial anti-inflammatory molecules (MAM), enhancement of epithelial barrier integrity, and modulation of pro- and anti-inflammatory cytokine responses. In contrast, A. muciniphila modulates mucosal immunity via Toll-like receptor 2 (TLR2) activation and tight junction enhancement but exhibits more variable patterns depending on disease and host context. This review offers an integrative framework comparing how these two taxa influence shared immune pathways such as the Th17/Treg axis, SCFA-G protein-coupled receptor (GPR) signaling, and epithelial barrier modulation across distinct autoimmune phenotypes. We also discuss therapeutic implications, including their roles as next-generation probiotics and the translational challenges of clinical application. By focusing on two mechanistically distinct but clinically relevant microbes, this review bridges current knowledge gaps and highlights promising directions for precision microbiome interventions in autoimmune diseases.

Decades of research have elucidated diverse aspects of neuroimmunology. This interdisciplinary field originates from the observation almost one century ago that local sensory signals in the skin regulate mast cell degranulation, a key event in allergic reactions. With this historical perspective, the current research has expanded in different dimensions, including hormonal mechanisms, direct immunomodulation by neural signals, and immune barriers in the central nervous system. Notably, neural innervations in the gastrointestinal tract can establish complex crosstalk with various immune cells through the release of specific neurotransmitters (e.g., norepinephrine or acetylcholine) or neuropeptides (e.g., calcitonin gene-related peptide), which engage the corresponding receptors expressed on immune cells (e.g., mast cells or innate lymphoid cells). Such neuroimmune interactions have become a frontier topic in biomedical science over the past years. In this review, we aim to summarize the current knowledge of neuroimmunology, with a focus on the gastrointestinal tract. We then highlight the implications of such neuroimmune interactions in the disease context of food allergy.

Chronic spontaneous urticaria (CSU) is characterized by recurrent wheals and/or angioedema without an identifiable trigger. Despite advances in therapy-including biologics such as omalizumab-suboptimal treatment adherence remains a major challenge, often resulting in poor symptom control and diminished quality of life. The objective of this study is to evaluate the existing literature on adherence in CSU and identify evidence-based strategies for improving long-term treatment engagement. A systematic literature search of PubMed and EMBASE was performed for articles published between 2000 and 2024 using the terms "chronic spontaneous urticaria," "chronic urticaria," "chronic idiopathic urticaria," "compliance," and "adherence." Eligible studies reported original data on adherence-related factors in CSU. Each study was categorized to World Health Organization (WHO) adherence dimensions: social/economic, healthcare system, condition-related, therapy-related, and patient-related. Risk of bias assessment was conducted for each study included in the final selection. The search followed PRISMA guidelines, and the protocol was registered with PROSPERO (ID: CRD42024627967). Twenty-one studies (totaling 18,500 patients) met inclusion criteria. Common barriers included lack of preventative medication use, inconvenience, forgetfulness, dissatisfaction with healthcare providers, and logistical challenges in accessing in-office biologic administration. Patients previously treated with immunosuppressants had a poorer response to omalizumab, which may contribute to nonadherence due to perceived lack of efficacy. External factors such as the COVID-19 pandemic also contributed to nonadherence by reducing clinic visits and access to specialist referrals. Higher education level and employment were significantly associated with improved adherence. Proposed strategies include simplifying treatment regimens, enhancing patient education about CSU chronicity, providing telehealth or home medication administration options, and offering financial or social support programs. Multiple interrelated barriers contribute to treatment nonadherence in patients with CSU, underscoring the need for multifaceted, patient-centered interventions. Clear communication, simplified regimens, and supportive resources may enhance adherence and help achieve improved long-term clinical outcomes.

Furry animals are familiar companions in modern society. Despite multiple beneficial roles in economic and social contexts, they can be the source of allergenic compounds. Moreover, research indicates that these allergens could be detected even in households where animals are not present. Consequently, the risk of asthma exacerbation is increased. Furthermore, accurately diagnosing a genuine allergy to furry animals remains a significant challenge for medical practitioners. Therefore, this review aims to gather and summarize valid information regarding three main groups of allergens associated with furry animals, including lipocalins, serum albumins, and secretoglobins. In this manuscript, we clarify the molecular structure of allergens, discuss cross-reactions between them, and highlight their clinical importance. We also outline the diagnostic techniques for furry animal allergy, as well as novel, emerging therapies. Additionally, we discuss the occupational risks of allergies for both laboratory workers and cattle farmers.

The aim of this study is to analyze data from all cases of Susac syndrome that have been published in the literature. This study was conducted in conformity with the PRISMA statement. A systematic review and survival analysis was performed for overall survival (OS) and progression-free survival (PFS). A total of 435 patients (males: 32.6%, n = 142), derived from 176 studies, were included in the analysis. The median age at diagnosis was 35 years (n = 433/435; range 7-69). Neurological symptoms were the most frequent (87.4%, n = 380/435). Among audio-vestibular symptoms (84.3%, n = 365/433), hearing loss was the most common manifestation (87.9%, n = 327/372). Branch retinal artery occlusions (BRAOs) were observed in 91.6% of patients (n = 261/285), while ophthalmological symptoms were reported in 78.9% (n = 288/365). The complete triad at onset was present in only 20.1% (n = 61/304) of cases. Complete recovery without sequelae was achieved in 59.5% (n = 44/74) of patients which reported neurological involvement, 39.7% (n = 27/68) of those with ophthalmological symptoms, and 17.7% (n = 11/62) of those with audio-vestibular symptoms. Partial recovery was observed in 36.5% (n = 27/74), 50.0% (n = 34/68), and 38.7% (n = 24/62) of patients, respectively. In a subgroup of 123 patients with available follow-up data (median duration: 12 months), 82.1% (n = 101) remained stable with controlled disease, 12.2% (n = 15) experienced a relapse, and 5.7% (n = 7) died. OS at 1 and 3 years was 94% (95% CI 88-97%). PFS was 89% at 1 year (95% CI: 80-94%) and 83% at 3 years (95% CI: 69-91%). Susac syndrome presents a significant clinical challenge. While presentations and outcomes are very heterogeneous, mortality is uncommon. The potential for relapse and long-term sequelae highlights the need for greater awareness and deeper understanding of the disease.

Asthma is a major chronic non-communicable respiratory disease, affecting over 300 million individuals globally, with an adult prevalence of 4.3%. Despite advances in individualized treatment, a subset of patients, particularly those with non-type 2 (non-T2) asthma, fails to achieve optimal disease control. Non-T2 asthma, characterized by steroid resistance and heterogeneous immune responses, remains a therapeutic challenge. Emerging evidence suggests that circadian rhythm disruption may modulate key pathological processes relevant to non-T2 asthma, including immune imbalance, epithelial barrier dysfunction, and impaired glucocorticoid sensitivity. This review investigates evidence of an association between circadian clock dysfunction and non-type 2 asthma pathogenesis, and proposes a hypothesis-driven framework to guide future studies. Chronotherapeutic strategies and clock-targeted interventions may offer promising avenues for future research and individualized treatment.