Clinical Reviews in Allergy & Immunology最新文献

{"title":"Targeting IL-33 and TSLP: A Novel Approach to Modulate Type 2 and Non-Type 2 Inflammatory Pathways in Pemphigus Vulgaris.","authors":"Gabriela Soto-Canetti, Brandon R Block, Jaanvi Mehta, Tammy Ehimwenma-Point Du Jour, Kristina Navrazhina, Jonas Adalsteinsson, Benjamin Ungar, Jordan Talia","doi":"10.1007/s12016-026-09181-3","DOIUrl":"10.1007/s12016-026-09181-3","url":null,"abstract":"<p><p>Pemphigus vulgaris (PV) is an autoantibody-mediated blistering disorder in which pathogenic immunoglobulins target epidermal desmoglein proteins, leading to suprabasal acantholysis that manifests clinically as flaccid blisters and mucosal erosions. First-line management typically includes oral corticosteroids as well as B-cell-depleting therapies such as rituximab; however, these and other systemic immunosuppressants carry substantial toxicities and are not suitable for all patients, motivating the search for more targeted, well-tolerated alternatives. Although PV is fundamentally driven by anti-desmoglein autoantibodies, emerging evidence implicates type 2 inflammation as a secondary contributor to disease activity, and epithelial-derived cytokines interleukin (IL)-33 and thymic stromal lymphopoietin (TSLP) have garnered interest as upstream modulators of this axis. Beyond canonical type 2 effects, IL-33 and TSLP can influence a broader inflammatory milieu, including modulating type 17 responses that may also contribute to PV immunopathology. No clinical evidence currently supports IL-33 or TSLP blockade in PV, and it remains to be determined if modulation of this secondary axis could potentially control disease as monotherapy. Nonetheless, given their upstream position in cutaneous immune processes, therapeutic blockade of IL-33 or TSLP warrants investigation in preclinical models and biomarker-informed trials, principally as an adjunct to current autoantibody-directed regimens.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tissue-Resident Macrophages: Linking Physiology and Inflammation in Infection.","authors":"Marcelo Eduardo Cardozo, Tatyane Martins Cirilo, Isabela de Brito Duval, Ana Laura Grossi de Oliveira, Luisa Mourão Dias Magalhães, Lilian Lacerda Bueno, Eric Dumonteil, Ricardo Toshio Fujiwara","doi":"10.1007/s12016-026-09195-x","DOIUrl":"10.1007/s12016-026-09195-x","url":null,"abstract":"<p><p>Macrophages are found in every tissue in the body, and their importance goes far beyond clearing pathogens. Developmental studies have shown that many macrophage populations originate during embryogenesis, persist through self-renewal, and adopt transcriptional and functional programs defined by their tissue environment. These tissue-resident macrophages (TRMs) are embedded within organ physiology, where they regulate, for instance, cardiac conduction, sculpt synaptic circuits, recycle iron, maintain epithelial barriers, and coordinate repair. During infection, TRMs connect to neural, metabolic, and structural circuits; therefore, inflammatory activation can alter organ function long after pathogen clearance. We propose that TRMs function as physiological integrators of immunity, translating local environmental cues into immune responses constrained by the demands of their tissue. This review examines macrophage populations across interconnected physiological systems, including the heart-brain axis, the spleen-liver network, and barrier tissues. In these settings, developmental origin, niche-derived signals, and metabolic programming determine how macrophages respond to infection and whether they preserve or disrupt tissue homeostasis. Additionally, we discuss how loss of resident identity during inflammatory stress contributes to chronic pathology and post-infectious sequelae and how emerging therapeutic strategies aim to restore tissue-specific macrophage programs. By framing immunity within organ physiology, we offer a conceptual model for understanding how infection reshapes tissue function through resident macrophages, as well as how targeting these cells could prevent long-term damage.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13569536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Signature and miRNA Pattern of CD4 + T Lymphocytes in Plaque Psoriasis.","authors":"Yelyzaveta Dubna, Katarzyna Nazimek","doi":"10.1007/s12016-026-09202-1","DOIUrl":"10.1007/s12016-026-09202-1","url":null,"abstract":"<p><p>Psoriasis is a global health problem affecting approximately 3% of the population. Because this autoimmune and autoinflammatory disease significantly reduces the quality of life and carries the risk of serious complications and comorbidities, all efforts have been directed towards developing effective therapeutic strategies that allow for a significant restoration of immunological homeostasis. To make this possible, basic research is being conducted, among others, to discover the molecular basis responsible for the pathogenic activation of autoreactive lymphocytes. At the same time, microRNAs seem to be very interesting candidates for epigenetic modulation of signaling pathways disturbed in psoriasis, which are themselves also affected in its pathogenesis. Therefore, our narrative review comprehensively summarizes the current knowledge on the molecular signature and miRNA profile that appear characteristic for psoriasis-related CD4 + T lymphocytes and hypothesizes the effects of microRNA dysregulation based on the results of a contextual functional analysis of selected candidates having the greatest impact on the pathogenesis of psoriasis. Detailed considerations allowed us to uncover the most important signaling pathways and microRNA molecules active in pathogenic CD4 + T lymphocytes that are involved in psoriasis progression, and also suggested other microRNAs that appear to have potential therapeutic activity, with the leading opposing roles of interferon regulatory factor 4, microRNA-155 and microRNA-150.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Climate Change-Mediated Temperature Extremes: Effects on the Immune System and Associations with Immune-Related Diseases.","authors":"Shengjie Li, Wenqu Tian, Yang Zheng, Yachun Li, Ismail Ogulur, Can Zeyneloglu, Huseyn Babayev, Mohamed Shamji, Kari Nadeau, Cezmi A Akdis, Yadong Gao","doi":"10.1007/s12016-026-09199-7","DOIUrl":"10.1007/s12016-026-09199-7","url":null,"abstract":"<p><p>Climate change exacerbates extreme temperature events, which pose a growing global threat to human health, especially disturbing the immune system and increasing the incidence of immune-related diseases. This review synthesizes the multifaceted links between extreme temperatures and human immune system. Extreme temperatures could activate the neuroendocrine system, trigger the release of cytokines, regulate heat shock proteins (HSPs) and induce epigenetic modifications. The epithelial barrier dysfunction and gut microbiota dysbiosis are involved in the association between extreme temperature and immune system. These immune perturbations increase the risk of allergic diseases, autoimmune disorders and infectious diseases, disproportionately affecting children, elderly, patients with chronic diseases and people living in low-income and geographically vulnerable areas. Noting limitations like insufficient focus on vulnerable groups and static models, this review highlights the urgency of addressing climate-temperature-immunity interactions to guide climate-resilient public health strategies.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epidemic Thunderstorm Asthma in China: A Systematic Review of an Artemisia-Associated Phenotype.","authors":"Le Cui, Xiaohong Lyu, Lauren Mazin, Zhenjing Geng, Rui Tang, Wei Zhao, Jinlyu Sun","doi":"10.1007/s12016-026-09194-y","DOIUrl":"10.1007/s12016-026-09194-y","url":null,"abstract":"<p><p>Epidemic thunderstorm asthma (ETSA) has historically been characterised around grass pollen in temperate Australia and Europe, whereas reports from northern China suggest an Artemisia-associated and potentially recurrent pattern. This systematic review synthesises primary evidence on the epidemiology, allergen profile, clinical features and early-warning systems of ETSA, comparing the Chinese and grass-pollen experiences. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 statement, PubMed, Web of Science, the China National Knowledge Infrastructure (CNKI) and Wanfang were searched to 30 June 2026, and reference lists were screened. Two reviewers independently selected studies, extracted data and assessed risk of bias with the Newcastle-Ottawa Scale and the Murad tool; certainty was rated using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. Because of clinical and methodological heterogeneity, no meta-analysis was performed. Of 436 records identified and 333 screened after de-duplication, 54 primary studies were included (43 international and 11 Chinese, spanning Yulin, Hohhot, Chongqing, Lanzhou and Shenzhen). Three recurring observational patterns were identified. Chinese reports, especially from northern and north-western China, frequently described mugwort (Artemisia) sensitisation rather than ryegrass sensitisation; the proportion without a prior asthma diagnosis was high in both settings (approximately 40% to 60% in China and up to 60% to 78% in Australian and United Kingdom cohorts); and recurrent events were reported at individual Chinese localities. Most Chinese reports used genus-level Artemisia or mugwort sensitisation and did not identify the airborne pollen to species. Evidence for direct Artemisia pollen rupture, pollution-related severity modification and pre-emptive treatment was low or very low. Priority research includes field aerosol sampling, prospective validation of locally calibrated warning systems, and trials of pre-emptive inhaled therapy.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impacts of Environmental Pollutants on Innate Immunity: The Role of Group 2 Innate Lymphoid Cells.","authors":"Yiting Luo, Wenjing He, Jing Li, Ruchong Chen","doi":"10.1007/s12016-026-09193-z","DOIUrl":"10.1007/s12016-026-09193-z","url":null,"abstract":"<p><p>Environmental pollution has emerged as one of the biggest threats to health in the contemporary world. Pollutants modify immune responses and may induce immunotoxicity. In this review, we describe the impact of significant environmental pollutants on the innate immune system, including ozone (O₃), particulate matter (PM), diesel exhaust particles (DEPs) and cigarette smoke (CS), as well as emerging pollutants such as chemical contaminants, nanomaterials, and microplastics, with a particular focus on the regulatory mechanisms of innate lymphoid cells (ILCs). ILCs, tissue-resident lymphocytes without antigen-specific receptors, have been demonstrated to be essential regulators linking environmental detection and immunological responses. Studies indicate that environmental pollutants activate ILCs and alter the immune responses by compromising the epithelial barrier and triggering the release of alarmins, including interleukin (IL)-33, IL-25, and thymic stromal lymphopoietin (TSLP). Among ILCs, group 2 innate lymphoid cells (ILC2s) are highly sensitive to pollutant-induced epithelial signals and play a critical role in type 2 inflammation. Beyond canonical alarmin signaling, accumulating evidence indicates that environmental pollutants regulate ILC2 biology thereby contributing to immune dysregulation and inflammatory diseases. A better understanding of how environmental pollutants regulate ILC2 activation, plasticity, and functional adaptation will facilitate the development of more precise preventive and therapeutic strategies for pollution-associated diseases.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From Barrier Disruption and Immune Dysregulation to Targeted Therapies in Atopic Dermatitis.","authors":"Xin Luo, Yichuan Li, Yinyi Feng, Ying Wang, Zhiyuan Li, Yong Zhang, Pan Shen","doi":"10.1007/s12016-026-09198-8","DOIUrl":"10.1007/s12016-026-09198-8","url":null,"abstract":"<p><p>Atopic dermatitis (AD) is a heterogeneous inflammatory skin disorder characterized by recurrent eczematous lesions and persistent pruritus. Its pathogenesis involves epidermal barrier dysfunction, immune dysregulation, microbial dysbiosis, and altered neuroimmune signaling. Genetic defects in structural proteins, particularly filaggrin, and altered epidermal lipids increase allergen and microbial penetration, perpetuating itch, scratching, tissue injury, and inflammation. Molecular evidence further reveals AD endotypes beyond conventional clinical phenotypes, with heterogeneity in immune polarization, barrier dysfunction, microbial colonization, and pruritic pathways. This heterogeneity may underlie differences in clinical presentation and treatment response. Conventional treatments, including skin hydration, antihistamines, and topical anti-inflammatory agents, often provide incomplete or transient control. Mechanism-based therapies targeting IL-4/IL-13, OX40/OX40L, JAK, and PDE4, together with AhR agonists, have broadened treatment options. However, efficacy must be balanced against treatment-specific risks. Biologics require monitoring for ocular and injection-site reactions, whereas systemic JAK inhibitors require monitoring for infections and laboratory abnormalities and carry regulatory class warnings regarding major adverse cardiovascular events, venous thromboembolism, and malignancy; however, these warnings are largely extrapolated from studies in older patients with rheumatoid arthritis, and the magnitude of these risks in patients with AD remains uncertain. Long-term safety and real-world evidence remain limited for several emerging therapies. This review synthesizes current knowledge of barrier dysfunction, immune heterogeneity, molecular endotypes, microbiome imbalance, neuroimmune signaling, and mechanism-based therapies. Integrating clinical phenotypes with molecular endotypes, predictive biomarkers, efficacy, and individualized safety assessment may enable more precise treatment selection and durable disease control.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond B cells: T and Innate Immune Mechanisms of Autoimmunity in Common Variable Immunodeficiency.","authors":"Paulina Kowalczyk, Katarzyna Zima, Natalia Sowa-Rogozińska, Monika Majewska-Szczepanik, Marcin Ziętkiewicz","doi":"10.1007/s12016-026-09197-9","DOIUrl":"10.1007/s12016-026-09197-9","url":null,"abstract":"<p><p>Common variable immunodeficiency (CVID) is the most prevalent symptomatic primary immunodeficiency, affecting approximately 1 in 25 000-50 000 individuals. Although classically characterized by hypogammaglobulinemia and recurrent bacterial infections, over 50% of patients develop non-infectious complications that constitute the major determinants of morbidity and mortality. The coexistence of immunodeficiency and immune dysregulation challenges the traditional B-cell-centric model of CVID pathogenesis. In this narrative review, we synthesize current evidence demonstrating that autoimmune manifestations in CVID arise from complex, multilayered immune dysfunction extending far beyond the B-cell compartment. Key abnormalities include Th1-skewed CD4⁺ T-cell responses with persistent IFN-γ production, numerical and functional defects in regulatory T cells, disruption of follicular T-cell subset balance favoring autoreactive germinal center responses, and progressive CD8⁺ T-cell exhaustion. At the innate immune level, NK-cell lymphopenia, constitutive monocyte activation, dendritic cell deficiency, neutrophil dysregulation, and proinflammatory innate lymphoid cell activity collectively contribute to the breakdown of self-tolerance. These immune perturbations are further amplified by systemic cytokine dysregulation. Pathogenic variants identified in patients with CVID-like disorders may further underlie autoimmune pathology and immune dysregulation, particularly those affecting T-cell co-stimulation, immune checkpoint signaling, NF-κB, and PI3K pathways. Collectively, CVID-associated autoimmunity represents a paradigm of systems-level immune dysregulation, underscoring the need for comprehensive immune phenotyping, genotype-informed stratification, and precision immunomodulatory strategies targeting the full spectrum of immune abnormalities involved.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13525027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148849956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rewiring Atopic Dermatitis: Alarmin Cytokines at the Core of Barrier-Immune-Neuro-Microbiome Networks.","authors":"Nafisah Oyinkansola Akim-Shittu, Ge Peng, Yi Tan, Alafate Abudouwanli, Quan Sun, Mengyao Yang, Wanchen Zhao, Hideoki Ogawa, Ko Okumura, François Niyonsaba","doi":"10.1007/s12016-026-09196-w","DOIUrl":"10.1007/s12016-026-09196-w","url":null,"abstract":"<p><p>Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by barrier dysfunction, type 2 immune dysregulation, pruritus, and microbial dysbiosis. Increasing evidence has revealed that epithelial-derived alarmin cytokines-thymic stromal lymphopoietin (TSLP), interleukin (IL)-33, and IL-25-are central upstream regulators that integrate structural damage with immune activation. These alarmin cytokines are rapidly induced by barrier stress and function at the epithelial-immune interface to orchestrate dendritic cell conditioning, group 2 innate lymphoid cell (ILC2) activation, T helper (Th) 2 polarization, and inflammatory memory. In addition to canonical immune amplification, alarmins directly modulate epidermal cell differentiation, antimicrobial responses, and neuro-immune circuits, thereby contributing to chronic itch, microbial imbalance, and relapse. Although TSLP, IL-33, and IL-25 exhibit overlapping functions, they operate in a coordinated and context-dependent manner. TSLP is predominantly a master regulator of adaptive type 2 immunity, IL-33 serves as a rapid innate immune amplifier and neuronal sensitizer, and IL-25 reinforces IL-13-dominant inflammatory circuits and memory-like ILC2 responses. Clinical trials targeting individual alarmins have reported strong biological rationales but variable efficacy in individuals with established moderate-to-severe AD, underscoring pathway integration and disease-stage specificity. This review synthesizes current advances in alarmin biology, including their cellular sources, receptor signaling, and roles in barrier dysfunction, dysbiosis, and neuroimmune crosstalk, as well as emerging clinical data. Understanding the context-specific functions of epithelial alarmins may inform the development of precision therapeutic strategies and redefine AD as a dynamic epithelial-immune disorder driven by upstream stress signaling networks.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148825627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global Asthma Disparities: Deciphering the Multifaceted Environmental Exposome Between Eastern and Western Populations.","authors":"Zhaowei Yang, Yuhan Xing, Xinru Wang, Weihua Peng, Xinliu Lin, Wenqing Yang, Jiayi Li, Qiyun Yang, Siyang Yao, Mo Xian, Zhongshan Gao, Yanmin Bao, Gary Wing-Kin Wong, Jing Li","doi":"10.1007/s12016-026-09191-1","DOIUrl":"10.1007/s12016-026-09191-1","url":null,"abstract":"<p><p>Early-life environmental exposures are critical determinants of the onset of childhood asthma, with risk patterns demonstrating significant heterogeneity across geographical and socioeconomic landscapes. While the \"hygiene hypothesis\" has long framed the rural-urban disparity-where urban children typically show higher asthma prevalence than their rural counterparts-this dichotomy is being reshaped by rapid globalization and urbanization. Furthermore, this pattern differs markedly between high-income countries (HICs) and low- and middle-income countries (LMICs). In HICs, the environmental distinction is sharp, with urban environments often characterized by a scarcity of protective microbial factors coupled with an accumulation of anthropogenic pollutants. In contrast, within developing economies undergoing rapid transition, the boundaries between rural and urban areas are increasingly blurred, and environmental exposures often involve a complex interaction among protective and risk factors. These divergent pathways are further complicated by socioeconomic inequities. This review summarizes the global burden of asthma, compares the multi-dimensional determinants across rural and urban environments in HICs (the West) and LMICs (the East), and constructs a refined risk map. It also seeks to identify key characteristics with potential for public health intervention, thereby providing a scientific basis for developing targeted asthma prevention strategies tailored to varying socioeconomic contexts.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"69 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}