Clinical Reviews in Allergy & Immunology最新文献

{"title":"Pathophysiology, Diagnosis, and Management of Chronic Spontaneous Urticaria: A Literature Review.","authors":"Benjamin Greiner,&nbsp;Savannah Nicks,&nbsp;Michael Adame,&nbsp;Jennifer McCracken","doi":"10.1007/s12016-022-08952-y","DOIUrl":"https://doi.org/10.1007/s12016-022-08952-y","url":null,"abstract":"<p><p>Chronic spontaneous urticaria (CSU) is characterized by recurring wheals that last 6 weeks or longer without an identifiable cause. The estimated point prevalence of CSU worldwide is 1%. Furthermore, it has a significant impact on quality of life in both adults and pediatric patients and their families. Although it is most often a self-limited disease, some patients have urticaria refractory to first-line treatment: second-generation H1 antihistamines. In these patients, the use of targeted monoclonal antibodies is necessary. While omalizumab is the only Food and Drug Administration-approved monoclonal antibody for CSU, others, including ligelizumab, dupilumab, benralizumab, and several orally administered Bruton's tyrosine kinase inhibitors, are also promising therapeutics for reducing the morbidity of CSU. Novel therapies, among others discussed here, are rapidly being developed with new trials and therapeutics being released nearly monthly. Thus, we performed a scoping literature review of randomized controlled trials studying targeted therapies for CSU. We also discuss the pathophysiology, diagnosis, prognosis, and future research directions in CSU.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40337416","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":"Systemic Sclerosis Association with Malignancy.","authors":"Gemma Lepri,&nbsp;Martina Catalano,&nbsp;Silvia Bellando-Randone,&nbsp;Serena Pillozzi,&nbsp;Elisa Giommoni,&nbsp;Roberta Giorgione,&nbsp;Cristina Botteri,&nbsp;Marco Matucci-Cerinic,&nbsp;Lorenzo Antonuzzo,&nbsp;Serena Guiducci","doi":"10.1007/s12016-022-08930-4","DOIUrl":"https://doi.org/10.1007/s12016-022-08930-4","url":null,"abstract":"<p><p>The association of systemic sclerosis (SSc) and cancer is well known from several decades suggesting common genetic and environmental risk factors involved in the development of both diseases. Immunosuppressive drugs widely used in SSc may increase the risk of cancer occurrence and different SSc clinical and serological features identify patients at major risk to develop malignancy. In this context, among serological features, presence of anti-RNA polymerase III and anti-topoisomerase I autoantibodies seems to increase cancer frequency in SSc patients (particularly lung and breast cancers). Lung fibrosis and a long standing SSc pulmonary involvement have been largely proposed as lung cancer risk factors, and the exposure to cyclophosphamide and an upper gastrointestinal involvement have been traditionally linked to bladder and oesophagus cancers, respectively. Furthermore, immune checkpoint inhibitors used for cancer therapy can induce immune-related adverse events, which are more frequent and severe in patients with pre-existing autoimmune diseases such as SSc. The strong association between SSc and cancer occurrence steers clinicians to carefully survey SSc patients performing periodical malignancy screening. In the present review, the most relevant bilateral relationships between SSc and cancer will be addressed.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9674744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40369493","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":"Hair Follicle Melanocytes Initiate Autoimmunity in Alopecia Areata: a Trigger Point.","authors":"Bo Xie,&nbsp;Jiayi Sun,&nbsp;Xiuzu Song","doi":"10.1007/s12016-022-08954-w","DOIUrl":"https://doi.org/10.1007/s12016-022-08954-w","url":null,"abstract":"<p><p>Alopecia areata (AA) is characterized by common non-scarring alopecia due to autoimmune disorders. To date, the specific pathogenesis underlying AA remains unknown. Thus, AA treatment in the dermatological clinic is still a challenge. Numerous clinical observations and experimental studies have established that melanocytes may be the trigger point that causes hair follicles to be attacked by the immune system. A possible mechanism is that the impaired melanocytes, under oxidative stress, cannot be repaired in time and causes apoptosis. Melanocyte-associated autoantigens are released and presented, inducing CD8⁺ T cell attacks. Thereafter, amplification of the immune responses further spreads to the entire hair follicle (HF). The immune privilege of HF subsequently collapses, leading to AA. Herein, we present a narrative review on the roles of melanocytes in AA pathogenesis, aiming to provide a better understanding of this disease from the melanocyte's perspective.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40369494","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 Genetics of Eczema Herpeticum.","authors":"Elisabeth Hodara,&nbsp;Peck Y Ong","doi":"10.1007/s12016-022-08953-x","DOIUrl":"https://doi.org/10.1007/s12016-022-08953-x","url":null,"abstract":"<p><p>Eczema herpeticum (EH) is a viral skin infection caused by herpes simplex virus (HSV) superimposed on eczematous skin lesions in atopic dermatitis (AD). Though the pathogenesis of EH has yet to be fully elucidated, the fact that EH is relatively rare despite a majority of adults showing serologic evidence of HSV exposure points to a genetic component predisposing to the disease. A number of genetic variants have been isolated in EH which may help distinguish a subgroup of patients susceptible to developing the condition. These unique genetic characteristics include deficiencies in skin barrier function and hydration, as well as at the level of the immune system. In this review, we summarize the genetic findings associated with EH identified to date. Isolating genetic markers in EH will be instrumental in stratifying patients at risk for EH and will have significant implications in the development and tailoring of targeted therapies.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40364577","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":"A Contemporary Update on the Diagnosis of Systemic Lupus Erythematosus.","authors":"Xin Huang,&nbsp;Qing Zhang,&nbsp;Huilin Zhang,&nbsp;Qianjin Lu","doi":"10.1007/s12016-021-08917-7","DOIUrl":"https://doi.org/10.1007/s12016-021-08917-7","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is a complicated autoimmune disease with female susceptibility. It is characterized by over-activation of the immune system and deposit of autoimmune complex in multiple organs. High heterogeneity, unpredictable disease course of SLE as well as the lack of specific and sensitive biomarkers posed diagnostic challenges to clinicians. Despite the complicated clinical presentation and pathogenesis of SLE, research regarding this disease has made many significant breakthroughs over the past decades. Some new learning can potentially be translated into clinical practice. In addition, new classification criteria to increase diagnostic accuracy were defined in 2019 by the European League Against Rheumatism/American College of Rheumatology (EULAR/ACR). Real-world studies have accumulated evidence for the adoption of this new classification criteria. Abundant classification criteria, improved recognition of organ-specific manifestations, and updated knowledge about lupus autoantibodies enable earlier diagnosis and more personalized medicine. Thus, it is important to update our knowledge about the latest clinical practices for lupus diagnosis. This review provides new insight into the diagnosis of SLE by summarizing recent advances in epidemiology, etiology, classification criteria, clinical manifestations, and study of autoantibodies.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39849017","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":"Thoracic Involvement in Systemic Autoimmune Rheumatic Diseases: Pathogenesis and Management.","authors":"Elena De Zorzi, Paolo Spagnolo, Elisabetta Cocconcelli, Elisabetta Balestro, Luca Iaccarino, Mariele Gatto, Francesco Benvenuti, Nicol Bernardinello, Andrea Doria, Toby M Maher, Elisabetta Zanatta","doi":"10.1007/s12016-022-08926-0","DOIUrl":"10.1007/s12016-022-08926-0","url":null,"abstract":"<p><p>Thoracic involvement is one of the main determinants of morbidity and mortality in patients with autoimmune rheumatic diseases (ARDs), with different prevalence and manifestations according to the underlying disease. Interstitial lung disease (ILD) is the most common pulmonary complication, particularly in patients with systemic sclerosis (SSc), idiopathic inflammatory myopathies (IIMs) and rheumatoid arthritis (RA). Other thoracic manifestations include pulmonary arterial hypertension (PAH), mostly in patients with SSc, airway disease, mainly in RA, and pleural involvement, which is common in systemic lupus erythematosus and RA, but rare in other ARDs.In this review, we summarize and critically discuss the current knowledge on thoracic involvement in ARDs, with emphasis on disease pathogenesis and management. Immunosuppression is the mainstay of therapy, particularly for ARDs-ILD, but it should be reserved to patients with clinically significant disease or at risk of progressive disease. Therefore, a thorough, multidisciplinary assessment to determine disease activity and degree of impairment is required to optimize patient management. Nevertheless, the management of thoracic involvement-particularly ILD-is challenging due to the heterogeneity of disease pathogenesis, the variety of patterns of interstitial pneumonia and the paucity of randomized controlled clinical trials of pharmacological intervention. Further studies are needed to better understand the pathogenesis of these conditions, which in turn is instrumental to the development of more efficacious therapies.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":null,"pages":null},"PeriodicalIF":8.4,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9674769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82434213","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":"Epigenetic Dysregulation in Autoimmune and Inflammatory Skin Diseases.","authors":"Frederick Gibson,&nbsp;Ailish Hanly,&nbsp;Nicole Grbic,&nbsp;Noah Grunberg,&nbsp;Muzhou Wu,&nbsp;Marianne Collard,&nbsp;Rhoda M Alani","doi":"10.1007/s12016-022-08956-8","DOIUrl":"https://doi.org/10.1007/s12016-022-08956-8","url":null,"abstract":"<p><p>Epigenetics is the study of heritable, reversible gene expression patterns that do not originate from alterations in the DNA sequence. Epigenetic modifications influence gene expression patterns and include DNA methylation, histone modifications, and gene regulation via non-coding RNAs. While the study of epigenetics has been most broadly applied to neoplastic diseases, the role of the epigenome in a wide range of disease processes including autoimmune, allergic, and inflammatory processes is increasingly being recognized. Recent advances in the study of the epigenome have led to novel insights into the pathogenesis and potential therapeutic targets of various pathologic entities including inflammatory diseases. In this review, we examine the nature of epigenetic modifications in several well-studied autoimmune, allergic, and/or inflammatory disorders of the skin including systemic lupus erythematosus, vitiligo, systemic sclerosis, alopecia areata, pemphigus, psoriasis, atopic dermatitis, keloidal scarring, and hidradenitis suppurativa with the aim to determine how such epigenetic changes may be targeted for therapeutic benefit.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40672538","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":"New Mechanistic Advances in FcεRI-Mast Cell-Mediated Allergic Signaling.","authors":"Yang Li,&nbsp;Patrick S C Leung,&nbsp;M Eric Gershwin,&nbsp;Junmin Song","doi":"10.1007/s12016-022-08955-9","DOIUrl":"https://doi.org/10.1007/s12016-022-08955-9","url":null,"abstract":"<p><p>Mast cells originate from the CD34⁺/CD117⁺ hematopoietic progenitors in the bone marrow, migrate into circulation, and ultimately mature and reside in peripheral tissues. Microbiota/metabolites and certain immune cells (e.g., Treg cells) play a key role in maintaining immune tolerance. Cross-linking of allergen-specific IgE on mast cells activates the high-affinity membrane-bound receptor FcεRI, thereby initiating an intracellular signal cascade, leading to degranulation and release of pro-inflammatory mediators. The intracellular signal transduction is intricately regulated by various kinases, transcription factors, and cytokines. Importantly, multiple signal components in the FcεRI-mast cell-mediated allergic cascade can be targeted for therapeutic purposes. Pharmacological interventions that include therapeutic antibodies against IgE, FcεRI, and cytokines as well as inhibitors/activators of several key intracellular signaling molecues have been used to inhibit allergic reactions. Other factors that are not part of the signal pathway but can enhance an individual's susceptibility to allergen stimulation are referred to as cofactors. Herein, we provide a mechanistic overview of the FcεRI-mast cell-mediated allergic signaling. This will broaden our scope and visions on specific preventive and therapeutic strategies for the clinical management of mast cell-associated hypersensitivity reactions.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9575623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33517269","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":"Autoantibodies and Cancer Association: the Case of Systemic Sclerosis and Dermatomyositis.","authors":"David F Fiorentino, Livia Casciola-Rosen","doi":"10.1007/s12016-022-08944-y","DOIUrl":"10.1007/s12016-022-08944-y","url":null,"abstract":"<p><p>Several rheumatic diseases have a perplexing association with cancer. Unraveling this mysterious connection is likely to provide deeper understanding regarding mechanisms governing the onset of both autoimmunity and cancer immunity, in addition to providing clinicians much needed guidance around whom and when to screen for occult malignancy. Systemic sclerosis (scleroderma) and dermatomyositis are two diseases in which the association with internal malignancy is well-described and can be considered as models from which to gain important insights that likely have broader applicability. The past 15 years have witnessed a striking acceleration in understanding how these two diseases are related to cancer emergence-an important crack in this inscrutable armor has been the discovery and characterization of disease-specific autoantigens that are closely tied with risk of cancer emergence. The best-described examples of this are antibodies against anti-RNA polymerase III (anti-POL3) and transcription intermediary factor 1-gamma (anti-TIF1γ). Patients with systemic sclerosis and cancer that are diagnosed within a short time interval of each other frequently have anti-POL3 antibodies. Antibodies against the minor spliceosome protein RNA-Binding Region Containing 3 (RNPC3) are also associated with increased cancer incidence in systemic sclerosis. Similarly, in the dermatomyositis spectrum, the majority of anti-TIF1γ-associated cancers are detected around the time of DM onset (most often within 1 year). Antibodies against Nuclear Matrix Protein 2 are also potentially associated with increased cancer emergence in dermatomyositis. The systemic sclerosis/anti-POL3 connection with close cancer onset led to the first experiments directly supporting the concept that rheumatic disease may in fact be a manifestation of cancer. It is now clear that studying these diseases through the lens of autoantibodies can reveal relationships and insights that would otherwise remain obscured. Extending these studies, new findings show that antibodies against RNA polymerase I large subunit are associated with protection against short interval cancers in anti-POL3-positive systemic sclerosis patients. These insights highlight the fact that autoantigen discovery related to cancer emergence remains an important priority; such new tools will enable the testing of specific hypotheses regarding mechanisms governing disease emergence and development of effective anti-tumor responses. Autoantibody phenotype will likely play an important role in the development of cancer screening guidelines that are critically needed by clinicians taking care of these patients. In this review, we will summarize the current state of knowledge regarding the different ways in which autoantibodies are connected with systemic sclerosis/dermatomyositis and malignancy and highlight potential paths forward.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10666558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82582657","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":"Antimitochondrial Antibodies: from Bench to Bedside.","authors":"Francesca Colapietro,&nbsp;Ana Lleo,&nbsp;Elena Generali","doi":"10.1007/s12016-021-08904-y","DOIUrl":"https://doi.org/10.1007/s12016-021-08904-y","url":null,"abstract":"<p><p>Anti-mitochondrial antibodies (AMA) are directed against the E2 subunits of the 2-oxo acid dehydrogenase complexes (PDC-E2) and are the typical biomarkers of primary biliary cholangitis (PBC), being present in 90-95% of patients, with increasing sensitivity at increasing titers. Albeit being highly specific for PBC diagnosis, AMA can be detected in less than 1% of healthy subjects, and thus the management subjects with no sign or symptom of liver disease is still a challenge and data concerning clinical risk of developing PBC in this subgroup of patients are controversial. Moreover, AMA can also be detected in patients affected by overlap syndrome, as well as hepatic diseases (i.e., NASH and viral hepatitis), while the association with autoimmune diseases, in particular Sjögren's syndrome, systemic sclerosis, and systemic lupus erythematosus, is well established. Furthermore, new associations are being identified with inflammatory myositis and heart disease. AMA are directed towards the pyruvate dehydrogenase multi enzyme complex (PDC-E2) subunit, which represents an epithelial specific autoantigen for PBC. This review focuses on the main characteristics of AMA, their association with autoimmune diseases and liver diseases.</p>","PeriodicalId":10423,"journal":{"name":"Clinical Reviews in Allergy & Immunology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8480115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10516050","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}