Clinical Reviews in Allergy & Immunology最新文献

{"title":"Th17 Response in Uveitis: A Double-Edged Sword in Ocular Inflammation and Immune Regulation.","authors":"Yuan Zong, Xue Tong, Wai Po Chong","doi":"10.1007/s12016-025-09038-1","DOIUrl":"10.1007/s12016-025-09038-1","url":null,"abstract":"<p><p>Uveitis involves a complex interplay of immune cell infiltration and cytokine imbalances, with Th17 cells playing a central role in this process. Th17 cells contribute to disease pathogenesis by promoting inflammation, recruiting additional immune cells, and directly damaging retinal tissues. This review discusses the current knowledge on therapeutic strategies targeting Th17-related cytokines, including cytokine blockade, small molecule inhibitors, and immunomodulatory approaches. Traditionally, Th17-related cytokines have been viewed as pro-inflammatory agents in uveitis. However, emerging research has highlighted the capacity of the Th17 response to express immunoregulatory cytokines, notably IL-10, IL-24, and TGF-β. This suggest that the Th17 response may have a dualistic role that includes immune suppression. In this review, we will discuss this paradoxical nature of Th17 cells in immune regulation and inflammation that they can both promote and mitigate uveitis. We expected that a deeper understanding of these mechanisms is imperative for the innovation of novel therapeutics that could consider the dual role of Th17 response in the pathogenesis of uveitis. By finely tuning the Th17 response to preserve retinal integrity and function, these new treatments could bring significant benefits to patients with uveitis. This review aims to shed light on the complexities of the Th17 response in uveitis and its implications for future therapeutic strategies.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"68 1","pages":"26"},"PeriodicalIF":8.4,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903535/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613584","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":"The Role of IL-17 in Systemic Autoinflammatory Diseases: Mechanisms and Therapeutic Perspectives.","authors":"Jingyuan Zhang, Min Shen","doi":"10.1007/s12016-025-09042-5","DOIUrl":"https://doi.org/10.1007/s12016-025-09042-5","url":null,"abstract":"<p><p>Interleukin (IL)-17, a pro-inflammatory cytokine, plays a pivotal role in immune regulation by bridging innate and adaptive responses. Beyond its canonical involvement in T helper-17 cells-mediated immunity, IL-17 contributes significantly to the pathogenesis of systemic autoinflammatory diseases (SAIDs) including Familial Mediterranean Fever (FMF), nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)-associated autoinflammatory diseases, and synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome. Dysregulated IL-17 signaling drives inflammasome activation, neutrophil recruitment, and chronic tissue inflammation. IL-17 inhibitors have demonstrated efficacy in refractory SAIDs, though challenges such as increased infection risks, paradoxical inflammatory reactions, and uncertainties regarding long-term safety persist. Currently, there is insufficient data to support the use of IL-17 inhibitors as first-line treatments, and their role in managing SAIDs is yet to be fully defined. This review highlights the mechanistic role of IL-17 in SAIDs and emerging therapeutic strategies, including IL-17-targeted monotherapies and combination approaches with IL-1 or tumor necrosis factor (TNF) inhibitors. Future research should focus on biomarker development, combination therapies, and long-term studies to optimize the safety and efficacy of IL-17-targeted therapies in SAIDs.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"68 1","pages":"27"},"PeriodicalIF":8.4,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613506","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":"The Role of Coagulation/Fibrinolysis Biomarkers in Pathophysiology, Disease Severity, and Treatment Response in Patients with Urticaria: A Scoping Review.","authors":"Hai-Yan Qin, Xian-Jun Xiao, Pei-Wen Xue, Di Qin, Si-Qi Wang, Ying Li, Yun-Zhou Shi, Li-Tao Pan","doi":"10.1007/s12016-025-09036-3","DOIUrl":"10.1007/s12016-025-09036-3","url":null,"abstract":"<p><p>The pathology of urticaria is complex. Recently, researchers have widely focused on the role that the coagulation/fibrinolysis system plays in the pathology of urticaria. The potential of coagulation/fibrinolysis biomarkers as disease severity or treatment response biomarkers remains uncertain, lacking comprehensive analysis in previous studies. Hence, we performed a scoping review to thoroughly analyze coagulation/fibrinolysis biomarkers that may predict disease progression and treatment response of urticaria. Data from 71 studies showed that chronic spontaneous urticaria (CSU) was the most-studied subtype (39 articles), with D-dimers being the most researched marker (56 articles). Twenty-one biomarkers were investigated, and ten biomarkers were significantly correlated with disease severity. Specifically, D-dimers (26 articles) and prothrombin fragment 1 + 2 (F₁₊₂) (12 articles) plasma levels increased with exacerbation and decreased with remission. Biomarkers such as D-dimer also correlated significantly with inflammatory cytokines and complement, suggesting interactions among coagulation, immunity, and inflammation in the pathology of urticaria. While these biomarkers may predict treatment response, more evidence is needed. Additionally, anticoagulants such as warfarin, heparin sodium and tranexamic acid have been proved effective for urticaria. This review emphasizes that some coagulation/fibrinolysis biomarkers (such as D-dimer and F₁₊₂) may be not only indicators of disease status but also potential predictors of treatment response. It aims to assist researchers and practitioners in gaining a better understanding of the close relationships among coagulation/fibrinolysis biomarkers, the condition of urticaria (especially chronic urticaria, CU), and its prognosis. It also provides new directions for future research on exploring treatment methods via the coagulation/fibrinolysis pathways.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"68 1","pages":"25"},"PeriodicalIF":8.4,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893642/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596358","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":"Hereditary Angioedema with Normal C1 Inhibitor: an Updated International Consensus Paper on Diagnosis, Pathophysiology, and Treatment.","authors":"Bruce L Zuraw, Konrad Bork, Laurence Bouillet, Sandra C Christiansen, Henriette Farkas, Anastasios E Germenis, Anete S Grumach, Allen Kaplan, Alberto López-Lera, Markus Magerl, Marc A Riedl, Adil Adatia, Aleena Banerji, Stephen Betschel, Isabelle Boccon-Gibod, Maria Bova, Henrik Balle Boysen, Teresa Caballero, Mauro Cancian, Anthony J Castaldo, Danny M Cohn, Deborah Corcoran, Christian Drouet, Atsushi Fukunaga, Michihiro Hide, Constance H Katelaris, Philip H Li, Hilary Longhurst, Jonny Peter, Fotis Psarros, Avner Reshef, Bruce Ritchie, Christine N Selva, Andrea Zanichelli, Marcus Maurer","doi":"10.1007/s12016-025-09027-4","DOIUrl":"10.1007/s12016-025-09027-4","url":null,"abstract":"<p><p>Hereditary angioedema (HAE) has been recognized for almost 150 years. The newest form of HAE, where C1 inhibitor levels are normal (HAE-nC1INH), was first described in 2000. Over the last two decades, new types of apparent non-mast cell-mediated angioedema with normal quantity and activity of C1INH have been described, in some cases with proven genetic pathogenic variants that co-segregate with angioedema expression within families. Like HAE due to C1INH deficiency, HAE-nC1INH patients are at risk of serious morbidity and mortality. Therefore, proactive management and treatment of HAE-nC1INH patients after an expert physician diagnosis is critically important. The underlying pathophysiology responsible for the angioedema has also been clarified in some of the HAE-nC1INH types. While several clinical guidelines and practice parameters including HAE-nC1INH have been published, we have made substantial progress in our understanding encompassing diagnostic criteria, pathophysiology, and treatment outcomes. HAE International (HAEi) and the US HAE Association (HAEA) convened a symposium of global HAE-nC1INH experts to synthesize our current knowledge in the area. Given the paucity of high-level evidence in HAE-nC1INH, all recommendations are based on expert opinion. This review and expert opinion on the best practice approach to diagnosing and treating HAE-nC1INH will support physicians to better manage patients with HAE-nC1INH.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"68 1","pages":"24"},"PeriodicalIF":8.4,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572262","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":"Review of the Pathophysiology and Clinical Manifestations of 22q11.2 Deletion and Duplication Syndromes.","authors":"Jeremy Purow, Lauren Waidner, Hanadys Ale","doi":"10.1007/s12016-025-09035-4","DOIUrl":"https://doi.org/10.1007/s12016-025-09035-4","url":null,"abstract":"<p><p>22q11.2 deletion and duplication syndromes are complex genetic syndromes composed of a wide spectrum of clinical manifestations, mostly affecting cardiovascular, endocrine, neurodevelopmental, and immune functioning. 22q11.2 deletion syndrome (22q11.2 DS) is more common and widely recognized compared to the duplication counterpart. Most of the literature focuses on delineating the genetic, molecular, and clinical impact of 22q11.2 DS, and less information focuses on the 22q11.2 duplication syndrome (22q11.2 DupS). We will cover both variants in this review and shed light on the less reported atypical 22q11.2 deletions and duplications. Variants in multiple genes in the 22q11.2 region, especially the TBX1 and DGCR8 genes, have been linked to the clinical phenotypes of 22q11.2 DS and 22q11.2 DupS. Variations in genes on the non-deleted homologous chromosome in the critical 22q11.2 region can further influence phenotypes by revealing recessive diseases. This effect has been documented for several genes in this area, such as SNAP29 and GP1BB. Neural crest development is usually impacted leading to various cardiovascular defects including Tetralogy of Fallot and truncus arteriosus. It can also cause palatal defects, especially velopharyngeal deficiency, considered another hallmark of 22q11DS. Individuals may also present with hypocalcemia and thyroid dysfunction due to impaired parathyroid gland formation and thyroid dysgenesis, respectively. Immunodeficiencies result from impaired T-cell development due to thymic hypoplasia, also a consequence of abnormal neural crest development. Humoral defects are also now increasingly recognized in these individuals. Psychiatric, neurocognitive, and developmental features are common, but severity varies across affected individuals. Other systems like the genitourinary, gastrointestinal, skeletal, and hematological are also involved. Monitoring and treating all the possible clinical manifestations require a multi-disciplinary approach to effectively address the plethora of clinical findings. The complex nature of the treatment guidelines reflects the clinical heterogeneity of these genetic variations. Further research is required to continue exploring the mechanisms relating to the impact of genetic aberrations in the 22q11.2 region on various clinical parameters. This will hopefully guide future updates to the current clinical practice guidelines to continue tailoring them to the individual needs of each affected person.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"68 1","pages":"23"},"PeriodicalIF":8.4,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556040","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":"Immune and Non-immune Interactions in the Pathogenesis of Androgenetic Alopecia.","authors":"Yu Xiao, Yi Zhang, Shuting Deng, Xueyuan Yang, Xu Yao","doi":"10.1007/s12016-025-09034-5","DOIUrl":"https://doi.org/10.1007/s12016-025-09034-5","url":null,"abstract":"<p><p>Androgenetic alopecia (AGA), a leading cause of progressive hair loss, affects up to 50% of males aged 50 years, causing significant psychological burden. Current treatments, such as anti-androgen drugs and minoxidil, show heterogeneous effects, even with long-term application. Meanwhile, the large-scale adoption of other adjuvant therapies has been slow, partly due to insufficient mechanistic evidence. A major barrier to developing better treatment for AGA is the incomplete understanding of its pathogenesis. The predominant academic consensus is that AGA is caused by abnormal expression of androgens and their receptors in individuals with a genetic predisposition. Emerging evidence suggests the contributing role of factors such as immune responses, oxidative stress, and microbiome changes, which were not previously given due consideration. Immune-mediated inflammation and oxidative stress disrupt hair follicles' function and damage the perifollicular niche, while scalp dysbiosis influences local metabolism and destabilizes the local microenvironment. These interconnected mechanisms collectively contribute to AGA pathogenesis. These additional aspects enhance our current understanding and confound the conventional paradigm, bridging the gap in developing holistic solutions for AGA. In this review, we gather existing evidence to discuss various etiopathogenetic factors involved in AGA and their possible interconnections, aiming to lay the groundwork for the future identification of therapeutic targets and drug development. Additionally, we summarize the advantages and disadvantages of AGA research models, ranging from cells and tissues to animals, to provide a solid basis for more effective mechanistic studies.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"68 1","pages":"22"},"PeriodicalIF":8.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536865","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":"Mesenchymal Stromal Cell-Based Therapy: A Promising Approach for Autoimmune Diseases.","authors":"Liming Li, Yong He, Junpeng Zhao, Huiqi Yin, Xiwei Feng, Xinyu Fan, Wei Wu, Qianjin Lu","doi":"10.1007/s12016-025-09030-9","DOIUrl":"https://doi.org/10.1007/s12016-025-09030-9","url":null,"abstract":"<p><p>Autoimmune diseases are characterized by immune dysregulation, resulting in aberrant reactivity of T cells and antibodies to self-antigens, leading to various patterns of inflammation and organ dysfunction. However, current therapeutic agents exhibit broad-spectrum activity and lack disease-specific selectivity, leading to enduring adverse effects, notably severe infections, and malignancies, and patients often fail to achieve the intended clinical goals. Mesenchymal stromal cells (MSCs) are multipotent stromal cells that can be easily derived from various tissues, such as adipose tissue, umbilical cords, Wharton's jelly, placenta, and dental tissues. MSCs offer advantages due to their immunomodulatory and anti-inflammatory abilities, low immunogenicity, and a high capacity for proliferation and multipotent differentiation, making them excellent candidates for cell-based treatment in autoimmune disorders. This review will cover preclinical studies and clinical trials involving MSCs in autoimmune diseases, as well as the primary challenges associated with the clinical application of MSC therapies and strategies for maximizing their therapeutic potential.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"68 1","pages":"21"},"PeriodicalIF":8.4,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467269","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":"Immunomodulatory Significance of Mast Cell Exosomes (MC-EXOs) in Immune Response Coordination.","authors":"Daniel Elieh-Ali-Komi, Farzaneh Shafaghat, Shamila D Alipoor, Tohid Kazemi, Dmitrii Atiakshin, Polina Pyatilova, Marcus Maurer","doi":"10.1007/s12016-025-09033-6","DOIUrl":"10.1007/s12016-025-09033-6","url":null,"abstract":"<p><p>Mast cells (MCs) communicate with other cells by direct cell-to-cell interaction, secreting mediators, and releasing exosomes (EXOs). MC-exosomes (MC-EXOs) contain proteins, lipids, mRNAs, and noncoding RNAs (ncRNAs), exhibit typical EXO markers such as heat shock proteins, tetraspanins, tumor susceptibility gene 101 protein (TSG101), and ALG-2-interacting protein X (ALIX), and are released constitutively or following MC degranulation. MC-EXOs also have signature MC markers like FcεRI and KIT (CD117), which allows for their identification and comparison with other EXO populations. Following their release, MC-EXOs may interact with the recipient cell(s) directly or be internalized and then release their protein and nucleic acid content. This may contribute to the regulation of immune responses and other biological processes and reprogramming of recipient cells. MC-EXO proteins may integrate and become a functional part of the recipient cell membrane. The mRNA transferred by MC-EXOs is functional and the transfer of exosomal RNA to other MCs results in the expression of donor MC proteins in the recipient MCs. Moreover, MCs may function as the recipients of EXOs that are released by other non-immune and immune cells, altering the secretome of MCs. In this review, we focus on how MC-EXOs modulate the biology of other cells and vice versa; and we highlight the role of MC-EXOs in the pathogenesis of allergic and non-allergic diseases.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"68 1","pages":"20"},"PeriodicalIF":8.4,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143457046","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":"Multi-omics in Allergic Rhinitis: Mechanism Dissection and Precision Medicine.","authors":"Yan Hao, Yujuan Yang, Hongfei Zhao, Ying Chen, Ting Zuo, Yu Zhang, Hang Yu, Limei Cui, Xicheng Song","doi":"10.1007/s12016-025-09028-3","DOIUrl":"10.1007/s12016-025-09028-3","url":null,"abstract":"<p><p>Allergic rhinitis (AR) is a common chronic inflammatory airway disease caused by inhaled allergens, and its prevalence has increased in recent decades. AR not only causes nasal leakage, itchy nose, nasal congestion, sneezing, and allergic conjunctivitis but also induces asthma, as well as sleep disorders, anxiety, depression, memory loss, and other phenomena that seriously affect the patient's ability to study and work, lower their quality of life, and burden society. The current methods used to diagnose and treat AR are still far from ideal. Multi-omics technology can be used to comprehensively and systematically analyze the differentially expressed DNA, RNA, proteins, and metabolites and their biological functions in patients with AR. These capabilities allow for an in-depth understanding of the intrinsic pathogenic mechanism of AR, the ability to explore key cells and molecules that drive its progression, and to design personalized treatment for AR. This article summarizes the progress made in studying AR by use of genomics, epigenomics, transcriptomics, proteomics, metabolomics, and microbiomics in order to illustrate the important role of multi-omics technologies in facilitating the precise diagnosis and treatment of AR.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"68 1","pages":"19"},"PeriodicalIF":8.4,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11836232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440082","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":"Age-Associated B Cells in Autoimmune Diseases: Pathogenesis and Clinical Implications.","authors":"Guangyang Xie, Xiaojing Chen, Yixia Gao, Ming Yang, Suqing Zhou, Liwei Lu, Haijing Wu, Qianjin Lu","doi":"10.1007/s12016-025-09021-w","DOIUrl":"10.1007/s12016-025-09021-w","url":null,"abstract":"<p><p>As a heterogeneous B cell subset, age-associated B cells (ABCs) exhibit distinct transcription profiles, extrafollicular differentiation processes, and multiple functions in autoimmunity. TLR7 and TLR9 signals, along with IFN-γ and IL-21 stimulation, are both essential for ABC differentiation, which is also regulated by chemokine receptors including CXCR3 and CCR2 and integrins including CD11b and CD11c. Given their functions in antigen uptake and presentation, autoantibody and proinflammatory cytokine secretion, and T helper cell activation, ABCs display potential in the prognosis, diagnosis, and therapy for autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome, multiple sclerosis, neuromyelitis optica spectrum disorders, and ankylosing spondylitis. Specifically targeting ABCs by inhibiting T-bet and CD11c and activating CD11b and ARA2 represents potential therapeutic strategies for SLE and RA. Although single-cell sequencing technologies have recently revealed the heterogeneous characteristics of ABCs, further investigations to explore and validate ABC-target therapies are still warranted.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":"68 1","pages":"18"},"PeriodicalIF":8.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11832777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440077","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}