Pub Date : 2026-02-08DOI: 10.1080/1744666X.2026.2625969
Ger T Rijkers, Zhibek Timraliyeva, Emma Mackie, Matei Lupuşoara
Introduction: Climate change and global warming have major consequences for human health, including effects on the immune system.
Areas covered: The impact of global warming on vector transmitted infectious diseases, such as West Nile Virus and dengue. Changes in pollen grain composition and pollen season duration, along with increased frequencies of dust storms, have detrimental impacts on asthmatic and allergic patients. The direct and indirect effects of climate change on autoimmune and cardiovascular diseases are also discussed. Literature on climate and the immune system was retrieved from PubMed and Google Scholar up to 21 July 2025.
Expert opinion: Climate change will lead to the spread of tropical infectious diseases toward moderate climate regions. Recommended vaccination schedules should be adapted to include these diseases. The changing climate has also extended pollen season and increased both the frequency and severity of dust storms, which impacts asthmatic patients. There are indications that next to extreme heath, pollen exposure contributes to acute cardiac events and complications after cardiovascular surgery. More insight into the underlying mechanisms of the negative effects of climate changes on the immune system could allow to take the appropriate measures and interventions to mitigate climate-associated immune-mediated diseases.
{"title":"Climate change and the immune system.","authors":"Ger T Rijkers, Zhibek Timraliyeva, Emma Mackie, Matei Lupuşoara","doi":"10.1080/1744666X.2026.2625969","DOIUrl":"10.1080/1744666X.2026.2625969","url":null,"abstract":"<p><strong>Introduction: </strong>Climate change and global warming have major consequences for human health, including effects on the immune system.</p><p><strong>Areas covered: </strong>The impact of global warming on vector transmitted infectious diseases, such as West Nile Virus and dengue. Changes in pollen grain composition and pollen season duration, along with increased frequencies of dust storms, have detrimental impacts on asthmatic and allergic patients. The direct and indirect effects of climate change on autoimmune and cardiovascular diseases are also discussed. Literature on climate and the immune system was retrieved from PubMed and Google Scholar up to 21 July 2025.</p><p><strong>Expert opinion: </strong>Climate change will lead to the spread of tropical infectious diseases toward moderate climate regions. Recommended vaccination schedules should be adapted to include these diseases. The changing climate has also extended pollen season and increased both the frequency and severity of dust storms, which impacts asthmatic patients. There are indications that next to extreme heath, pollen exposure contributes to acute cardiac events and complications after cardiovascular surgery. More insight into the underlying mechanisms of the negative effects of climate changes on the immune system could allow to take the appropriate measures and interventions to mitigate climate-associated immune-mediated diseases.</p>","PeriodicalId":12175,"journal":{"name":"Expert Review of Clinical Immunology","volume":" ","pages":"1-17"},"PeriodicalIF":3.7,"publicationDate":"2026-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146104184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-08DOI: 10.1080/1744666X.2026.2625964
Ioannis Parodis, Dionysis Nikolopoulos, André Brylid, Olof Hultgren, Marta E Alarcón-Riquelme, Christopher Sjöwall
Introduction: Systemic lupus erythematosus (SLE) is a prototypical autoimmune disorder characterized by production of autoantibodies targeting self-antigens. These autoantibodies form immune-complexes that deposit in various tissues, leading to complement activation, inflammation, and, ultimately, organ damage. The detection of specific autoantibodies is crucial for diagnosing SLE and for assessing disease activity.
Areas covered: A variety of autoantibodies are employed in clinical practice to assess the risk of different SLE manifestations and other systemic inflammatory diseases. These autoantibody specificities are integral to clinical decision-making procedures. Herein, we examine the most commonly evaluated autoantibodies and their associations with disease phenotypes. In addition, we discuss recent findings of novel autoantibodies in SLE and their clinical relevance and potential utility.
Expert opinion: In addition to the well-established autoantibody specificities routinely assessed in clinical practice for patients with a diagnosis of - or clinically suspected - SLE, recent studies have identified several new autoantibodies with potential clinical relevance. If these findings are validated through further research and accessible diagnostic assays are developed, these emerging autoantibodies could narrow the gap between first symptoms and classifiable disease and significantly enhance patient management by providing critical insights into the risk of specific SLE manifestations, thereby facilitating more timely and personalized interventions.
{"title":"Old and new autoantibodies in systemic lupus erythematosus.","authors":"Ioannis Parodis, Dionysis Nikolopoulos, André Brylid, Olof Hultgren, Marta E Alarcón-Riquelme, Christopher Sjöwall","doi":"10.1080/1744666X.2026.2625964","DOIUrl":"10.1080/1744666X.2026.2625964","url":null,"abstract":"<p><strong>Introduction: </strong>Systemic lupus erythematosus (SLE) is a prototypical autoimmune disorder characterized by production of autoantibodies targeting self-antigens. These autoantibodies form immune-complexes that deposit in various tissues, leading to complement activation, inflammation, and, ultimately, organ damage. The detection of specific autoantibodies is crucial for diagnosing SLE and for assessing disease activity.</p><p><strong>Areas covered: </strong>A variety of autoantibodies are employed in clinical practice to assess the risk of different SLE manifestations and other systemic inflammatory diseases. These autoantibody specificities are integral to clinical decision-making procedures. Herein, we examine the most commonly evaluated autoantibodies and their associations with disease phenotypes. In addition, we discuss recent findings of novel autoantibodies in SLE and their clinical relevance and potential utility.</p><p><strong>Expert opinion: </strong>In addition to the well-established autoantibody specificities routinely assessed in clinical practice for patients with a diagnosis of - or clinically suspected - SLE, recent studies have identified several new autoantibodies with potential clinical relevance. If these findings are validated through further research and accessible diagnostic assays are developed, these emerging autoantibodies could narrow the gap between first symptoms and classifiable disease and significantly enhance patient management by providing critical insights into the risk of specific SLE manifestations, thereby facilitating more timely and personalized interventions.</p>","PeriodicalId":12175,"journal":{"name":"Expert Review of Clinical Immunology","volume":" ","pages":"1-11"},"PeriodicalIF":3.7,"publicationDate":"2026-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-04DOI: 10.1080/1744666X.2026.2625970
Simone Appenzeller, Paulo Rogerio Julio, Rodrigo Marchi Silva, Stephanie K A Wong, Marinka Twilt
Introduction: Inflammatory brain diseases (IBrainDs) are rare, potentially devastating diseases that affect children and adolescents. Clinical presentation is often subacute with focal and diffuse neurological manifestations and psychiatric symptoms which may occur without early aggressive treatment.
Areas covered: In this review performed in Pubmed including English Literature until July 2025 on the different IBrainDs categories include the clinical presentation, laboratory features, treatment, and outcome of these IBrainDs.
Expert opinion: As IBrainDs often present subacute and insidious, a high index of suspicion is warranted as often CSF and MRI findings are nonspecific and specific antibody testing, angiography, or brain biopsy are necessary to confirm the diagnosis. Here we will review the main categories of IBrainDs, clinical presentation, and discuss pathophysiologic mechanisms to support treatment choices.
{"title":"Translational approaches to childhood inflammatory brain diseases: a review.","authors":"Simone Appenzeller, Paulo Rogerio Julio, Rodrigo Marchi Silva, Stephanie K A Wong, Marinka Twilt","doi":"10.1080/1744666X.2026.2625970","DOIUrl":"10.1080/1744666X.2026.2625970","url":null,"abstract":"<p><strong>Introduction: </strong>Inflammatory brain diseases (IBrainDs) are rare, potentially devastating diseases that affect children and adolescents. Clinical presentation is often subacute with focal and diffuse neurological manifestations and psychiatric symptoms which may occur without early aggressive treatment.</p><p><strong>Areas covered: </strong>In this review performed in Pubmed including English Literature until July 2025 on the different IBrainDs categories include the clinical presentation, laboratory features, treatment, and outcome of these IBrainDs.</p><p><strong>Expert opinion: </strong>As IBrainDs often present subacute and insidious, a high index of suspicion is warranted as often CSF and MRI findings are nonspecific and specific antibody testing, angiography, or brain biopsy are necessary to confirm the diagnosis. Here we will review the main categories of IBrainDs, clinical presentation, and discuss pathophysiologic mechanisms to support treatment choices.</p>","PeriodicalId":12175,"journal":{"name":"Expert Review of Clinical Immunology","volume":" ","pages":"1-14"},"PeriodicalIF":3.7,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146092182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of morbidity and mortality worldwide, with type 2 diabetes mellitus (T2DM), obesity and cardiovascular disease being common co-morbidities associated with worse outcomes. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter-2 (SGLT2) inhibitors which were originally developed for treatment of T2DM and/or obesity, have recently been shown to reduce exacerbations in observational studies of patients with COPD, suggesting that repurposing GLP-1RAs and SGLT2 inhibitors could improve clinical outcomes in COPD.
Areas covered: COPD, diabetes and obesity share several common inflammatory pathways, including macrophage dysfunction, inflammasome activation and metabolic dysregulation. Here we review the pharmacology, pre-clinical and emerging clinical data which could support repurposing of GLP-1RAs and SGLT2 inhibitors for use in COPD through a search of articles in PubMed and Medline from 01/1950 to 08/2025.
Expert opinion: Reevaluating metabolic therapeutic targets has the potential to redefine treatment strategies for patients with COPD and metabolic comorbidities. Potential mechanisms of action could be via modulation of the NLRP3 inflammasome and macrophage polarization or better control of co-morbid conditions. However, randomized controlled trials and mechanistic studies are needed to confirm these observational findings and elucidate underlying mechanisms.
{"title":"The role of glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter-2 inhibitors in Chronic obstructive pulmonary disease.","authors":"Jordina Sy Mah, Pei Chia Eng, Chioma Izzi-Engbeaya, Lydia J Finney","doi":"10.1080/1744666X.2026.2625967","DOIUrl":"https://doi.org/10.1080/1744666X.2026.2625967","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of morbidity and mortality worldwide, with type 2 diabetes mellitus (T2DM), obesity and cardiovascular disease being common co-morbidities associated with worse outcomes. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter-2 (SGLT2) inhibitors which were originally developed for treatment of T2DM and/or obesity, have recently been shown to reduce exacerbations in observational studies of patients with COPD, suggesting that repurposing GLP-1RAs and SGLT2 inhibitors could improve clinical outcomes in COPD.</p><p><strong>Areas covered: </strong>COPD, diabetes and obesity share several common inflammatory pathways, including macrophage dysfunction, inflammasome activation and metabolic dysregulation. Here we review the pharmacology, pre-clinical and emerging clinical data which could support repurposing of GLP-1RAs and SGLT2 inhibitors for use in COPD through a search of articles in PubMed and Medline from 01/1950 to 08/2025.</p><p><strong>Expert opinion: </strong>Reevaluating metabolic therapeutic targets has the potential to redefine treatment strategies for patients with COPD and metabolic comorbidities. Potential mechanisms of action could be via modulation of the NLRP3 inflammasome and macrophage polarization or better control of co-morbid conditions. However, randomized controlled trials and mechanistic studies are needed to confirm these observational findings and elucidate underlying mechanisms.</p>","PeriodicalId":12175,"journal":{"name":"Expert Review of Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-03DOI: 10.1080/1744666X.2026.2621811
Olha Kharasakhal, John Maher
Introduction: Management of inoperable and advanced malignant melanoma has been transformed in recent years by the advent of a number of approaches, including immune checkpoint blockade, small-molecule inhibitors, and adoptive immunotherapy with ex vivo expanded tumor-infiltrating lymphocytes.
Areas covered: In this review, we describe efforts made to develop an alternative immunotherapeutic approach for this disease using chimeric antigen receptor (CAR) engineered T-cells. Literature was reviewed in the PubMed database and clinicaltrials.gov website (1998-2025).
Expert opinion: CAR T-cell immunotherapy has proven transformative in the treatment of selected hematological malignancies. However, solid tumors such as melanoma remain much more challenging to treat using this emerging modality. Here we consider issues surrounding target selection, encompassing both tumor cells and accompanying stroma, in addition to armoring approaches that may potentiate delivery to or efficacy within the tumor microenvironment. We also consider a number of advanced CAR-based architectures to enable multi-antigen or universal antigen targeting and combination-based approaches.
{"title":"CAR-T cell immunotherapy of malignant melanoma.","authors":"Olha Kharasakhal, John Maher","doi":"10.1080/1744666X.2026.2621811","DOIUrl":"10.1080/1744666X.2026.2621811","url":null,"abstract":"<p><strong>Introduction: </strong>Management of inoperable and advanced malignant melanoma has been transformed in recent years by the advent of a number of approaches, including immune checkpoint blockade, small-molecule inhibitors, and adoptive immunotherapy with ex vivo expanded tumor-infiltrating lymphocytes.</p><p><strong>Areas covered: </strong>In this review, we describe efforts made to develop an alternative immunotherapeutic approach for this disease using chimeric antigen receptor (CAR) engineered T-cells. Literature was reviewed in the PubMed database and clinicaltrials.gov website (1998-2025).</p><p><strong>Expert opinion: </strong>CAR T-cell immunotherapy has proven transformative in the treatment of selected hematological malignancies. However, solid tumors such as melanoma remain much more challenging to treat using this emerging modality. Here we consider issues surrounding target selection, encompassing both tumor cells and accompanying stroma, in addition to armoring approaches that may potentiate delivery to or efficacy within the tumor microenvironment. We also consider a number of advanced CAR-based architectures to enable multi-antigen or universal antigen targeting and combination-based approaches.</p>","PeriodicalId":12175,"journal":{"name":"Expert Review of Clinical Immunology","volume":" ","pages":"1-17"},"PeriodicalIF":3.7,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146060960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-03DOI: 10.1080/1744666X.2026.2625277
Tomohiro Koga
Introduction: Autoinflammatory diseases are inherited disorders of innate immunity, broadly classified into inflammasomopathies, interferonopathies, and complement-mediated disorders. They are characterized by dysregulated cytokine signaling - particularly IL-1, IL-6, TNF, type I interferon, and the JAK-STAT pathway-and are increasingly managed with molecular targeted therapies. Prototypical entities include familial Mediterranean fever (FMF), TNF receptor - associated periodic syndrome (TRAPS), and cryopyrin-associated periodic syndromes (CAPS). Other conditions - notably mevalonate kinase deficiency (MKD/HIDS), deficiency of adenosine deaminase 2 (DADA2), haploinsufficiency of A20 (HA20), OTULIN-related autoinflammatory syndromes, and proteasome-associated autoinflammatory syndromes (PRAAS) - are now recognized as biologic-responsive diseases.
Areas covered: This review summarizes molecular mechanisms and therapeutic strategies, focusing on IL-1 blockade with anakinra, canakinumab, and rilonacept, as well as IL-6 and TNF inhibitors, integrating evidence from clinical trials and real-world studies.
Expert opinion: IL-1 inhibition has transformed the management of inflammasome-mediated diseases, enabling glucocorticoid-free remission and reducing amyloidosis risk. TNF inhibitors remain standard for vasculopathic disorders such as DADA2, while IL-6 blockade and JAK inhibitors are options in selected refractory cases. The recognition of novel syndromes, including HA20, OTULIN deficiency, and PRAAS, has broadened the therapeutic landscape, and next-generation biologics may further enable personalized treatment.
{"title":"Targeting cytokine pathways: the role of biologics in autoinflammatory disorders.","authors":"Tomohiro Koga","doi":"10.1080/1744666X.2026.2625277","DOIUrl":"10.1080/1744666X.2026.2625277","url":null,"abstract":"<p><strong>Introduction: </strong>Autoinflammatory diseases are inherited disorders of innate immunity, broadly classified into inflammasomopathies, interferonopathies, and complement-mediated disorders. They are characterized by dysregulated cytokine signaling - particularly IL-1, IL-6, TNF, type I interferon, and the JAK-STAT pathway-and are increasingly managed with molecular targeted therapies. Prototypical entities include familial Mediterranean fever (FMF), TNF receptor - associated periodic syndrome (TRAPS), and cryopyrin-associated periodic syndromes (CAPS). Other conditions - notably mevalonate kinase deficiency (MKD/HIDS), deficiency of adenosine deaminase 2 (DADA2), haploinsufficiency of A20 (HA20), OTULIN-related autoinflammatory syndromes, and proteasome-associated autoinflammatory syndromes (PRAAS) - are now recognized as biologic-responsive diseases.</p><p><strong>Areas covered: </strong>This review summarizes molecular mechanisms and therapeutic strategies, focusing on IL-1 blockade with anakinra, canakinumab, and rilonacept, as well as IL-6 and TNF inhibitors, integrating evidence from clinical trials and real-world studies.</p><p><strong>Expert opinion: </strong>IL-1 inhibition has transformed the management of inflammasome-mediated diseases, enabling glucocorticoid-free remission and reducing amyloidosis risk. TNF inhibitors remain standard for vasculopathic disorders such as DADA2, while IL-6 blockade and JAK inhibitors are options in selected refractory cases. The recognition of novel syndromes, including HA20, OTULIN deficiency, and PRAAS, has broadened the therapeutic landscape, and next-generation biologics may further enable personalized treatment.</p>","PeriodicalId":12175,"journal":{"name":"Expert Review of Clinical Immunology","volume":" ","pages":"1-15"},"PeriodicalIF":3.7,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-03DOI: 10.1080/1744666X.2026.2625281
Albert Gil-Vila, Ernesto Trallero-Araguás, Clara Edo-Fernandez, Iago Pinal-Fernandez, Aitor Uribarri, Hug Cuellar-Calabria, Albert Selva-O'Callaghan
Introduction: Inflammatory myopathies (IM) are a heterogeneous group of systemic disorders characterized by chronic muscle inflammation. Cardiac involvement has historically been underrecognized, partially because of its subclinical presentation, and is associated with a poor prognosis, underscoring the urgent need for effective diagnostic strategies and therapeutic approaches. Cardiac magnetic resonance and its new mapping techniques appear as one of the most valuable instruments to detect myocardial involvement, thereby limiting the need for an endomyocardial biopsy when the underlying cause of cardiac dysfunction is unclear or when noninvasive imaging is inconclusive. Evidence-based data remains lacking regarding treatment strategies, and nowadays, immunosuppressive therapy constitutes the cornerstone of treatment.
Areas covered: In this review, we provide a summary of the current literature on myocarditis in the context of IM, with a focus on clinical manifestations, underlying pathophysiological mechanisms, diagnostic methods, and therapeutic strategies.
Expert opinion: We are currently in a privileged moment regarding IM, as there has never been a time with so many ongoing clinical trials. With growing awareness of cardiac involvement in IM, now is the time to focus research efforts on cardiac involvement in IM to address this underrecognized manifestation that carries significant morbidity and prognostic implications in patients with IM.
{"title":"Myocardial involvement in inflammatory myopathies: from subclinical disease to life-threatening myocarditis.","authors":"Albert Gil-Vila, Ernesto Trallero-Araguás, Clara Edo-Fernandez, Iago Pinal-Fernandez, Aitor Uribarri, Hug Cuellar-Calabria, Albert Selva-O'Callaghan","doi":"10.1080/1744666X.2026.2625281","DOIUrl":"10.1080/1744666X.2026.2625281","url":null,"abstract":"<p><strong>Introduction: </strong>Inflammatory myopathies (IM) are a heterogeneous group of systemic disorders characterized by chronic muscle inflammation. Cardiac involvement has historically been underrecognized, partially because of its subclinical presentation, and is associated with a poor prognosis, underscoring the urgent need for effective diagnostic strategies and therapeutic approaches. Cardiac magnetic resonance and its new mapping techniques appear as one of the most valuable instruments to detect myocardial involvement, thereby limiting the need for an endomyocardial biopsy when the underlying cause of cardiac dysfunction is unclear or when noninvasive imaging is inconclusive. Evidence-based data remains lacking regarding treatment strategies, and nowadays, immunosuppressive therapy constitutes the cornerstone of treatment.</p><p><strong>Areas covered: </strong>In this review, we provide a summary of the current literature on myocarditis in the context of IM, with a focus on clinical manifestations, underlying pathophysiological mechanisms, diagnostic methods, and therapeutic strategies.</p><p><strong>Expert opinion: </strong>We are currently in a privileged moment regarding IM, as there has never been a time with so many ongoing clinical trials. With growing awareness of cardiac involvement in IM, now is the time to focus research efforts on cardiac involvement in IM to address this underrecognized manifestation that carries significant morbidity and prognostic implications in patients with IM.</p>","PeriodicalId":12175,"journal":{"name":"Expert Review of Clinical Immunology","volume":" ","pages":"1-14"},"PeriodicalIF":3.7,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146104190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: This meta-analysis evaluates the risk of all-cause and cause-specific mortality in patients with atopic dermatitis (AD).
Methods: A systematic search of PubMed, EMBASE, and the Cochrane Library (from inception to April 2025) was conducted for cohort studies comparing mortality risks in AD patients versus controls, in accordance with PRISMA guidelines. Two reviewers screened studies, extracted data, and assessed quality using the Newcastle-Ottawa Scale. Hazard ratios (HRs) were calculated using random-effects models in Stata 14.0, with sensitivity analyses, subgroup analyses, and publication bias assessments.
Results: Nine cohort studies were included. AD patients had significantly increased risks of all-cause mortality [HR = 1.222, 95% CI (1.117-1.336)], as well as mortality due to infectious diseases [HR = 1.606, CI (1.087-2.372)], cancer [HR = 1.129, CI (1.015-1.256)], respiratory diseases [HR = 1.381, CI (1.044-1.825)], and gastrointestinal diseases [HR = 1.658, CI (1.002-2.743)]. Subgroup analyses revealed a higher risk of all-cause mortality in prospective studies compared to retrospective studies, with significantly higher risks in studies from Europe and Asia.
Conclusions: AD is associated with an elevated risk of all-cause and cause-specific mortality, underscoring the need for improved monitoring and targeted interventions. Future research should incorporate more diverse populations and study designs.
{"title":"All-cause and cause-specific mortality in atopic dermatitis patients: a systematic review and meta-analysis.","authors":"Yi Yang, Qin Zhang, Jinpeng Zhao, Anning Huang, Jianren Yang, Lulu Wang, Yuan Zeng, Guomei Xu","doi":"10.1080/1744666X.2026.2618271","DOIUrl":"10.1080/1744666X.2026.2618271","url":null,"abstract":"<p><strong>Introduction: </strong>This meta-analysis evaluates the risk of all-cause and cause-specific mortality in patients with atopic dermatitis (AD).</p><p><strong>Methods: </strong>A systematic search of PubMed, EMBASE, and the Cochrane Library (from inception to April 2025) was conducted for cohort studies comparing mortality risks in AD patients versus controls, in accordance with PRISMA guidelines. Two reviewers screened studies, extracted data, and assessed quality using the Newcastle-Ottawa Scale. Hazard ratios (HRs) were calculated using random-effects models in Stata 14.0, with sensitivity analyses, subgroup analyses, and publication bias assessments.</p><p><strong>Results: </strong>Nine cohort studies were included. AD patients had significantly increased risks of all-cause mortality [HR = 1.222, 95% CI (1.117-1.336)], as well as mortality due to infectious diseases [HR = 1.606, CI (1.087-2.372)], cancer [HR = 1.129, CI (1.015-1.256)], respiratory diseases [HR = 1.381, CI (1.044-1.825)], and gastrointestinal diseases [HR = 1.658, CI (1.002-2.743)]. Subgroup analyses revealed a higher risk of all-cause mortality in prospective studies compared to retrospective studies, with significantly higher risks in studies from Europe and Asia.</p><p><strong>Conclusions: </strong>AD is associated with an elevated risk of all-cause and cause-specific mortality, underscoring the need for improved monitoring and targeted interventions. Future research should incorporate more diverse populations and study designs.</p><p><strong>Prospero identifier: </strong>CRD420251038553.</p>","PeriodicalId":12175,"journal":{"name":"Expert Review of Clinical Immunology","volume":" ","pages":"1-9"},"PeriodicalIF":3.7,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146009502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-21DOI: 10.1080/1744666X.2026.2620427
Giuseppe Guido Maria Scarlata, Ludovico Abenavoli
{"title":"The role of gut microbiota in the pathogenesis of primary biliary cholangitis: an immunological perspective.","authors":"Giuseppe Guido Maria Scarlata, Ludovico Abenavoli","doi":"10.1080/1744666X.2026.2620427","DOIUrl":"10.1080/1744666X.2026.2620427","url":null,"abstract":"","PeriodicalId":12175,"journal":{"name":"Expert Review of Clinical Immunology","volume":" ","pages":"1-4"},"PeriodicalIF":3.7,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146009453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: Obstetric antiphospholipid syndrome (OAPS) is a complex autoimmune disorder that contributes significantly to pregnancy morbidity. Despite advances in understanding its mechanisms, 20-30% of women, especially those refractory to standard treatments, continue to face adverse outcomes. Emerging therapies, including biologics and immunomodulators, are under investigation; however, data in this field remain limited.
Areas covered: This review examines the current understanding of OAPS pathogenesis and risk stratification. It evaluates established management strategies such as aspirin and heparin, and explores adjunctive or investigational therapies, including hydroxychloroquine, corticosteroids, intravenous immunoglobulins, statins, plasma exchange, and biologics. Key knowledge gaps, concerning refractory cases and personalized treatment approaches, are highlighted, emphasizing the importance of multidisciplinary, risk-based care throughout preconception, pregnancy, and postpartum. This review focuses primarily on primary OAPS rather than secondary APS associated with systemic lupus erythematosus.
Expert opinion: Innovations in immunotherapy and targeted biologics hold promise for refractory OAPS; however, large trials are needed to confirm their safety and efficacy during pregnancy. Future management is likely to involve biomarker-driven strategies, incorporating machine learning to enhance prediction and individualization of treatment. The development of standardized diagnostic criteria and risk assessment tools, alongside multidisciplinary collaboration, will be crucial in advancing care, ultimately transforming maternal-fetal health outcomes.
{"title":"Navigating obstetric antiphospholipid syndrome: pathophysiology, diagnosis, and therapeutic advances.","authors":"Ghaydaa Aldabie, Ahlam Almarzooqi, Roaa Aljohani, Manar Altawash, Amjad Alkadi, Munther Khamashta","doi":"10.1080/1744666X.2025.2612589","DOIUrl":"10.1080/1744666X.2025.2612589","url":null,"abstract":"<p><strong>Introduction: </strong>Obstetric antiphospholipid syndrome (OAPS) is a complex autoimmune disorder that contributes significantly to pregnancy morbidity. Despite advances in understanding its mechanisms, 20-30% of women, especially those refractory to standard treatments, continue to face adverse outcomes. Emerging therapies, including biologics and immunomodulators, are under investigation; however, data in this field remain limited.</p><p><strong>Areas covered: </strong>This review examines the current understanding of OAPS pathogenesis and risk stratification. It evaluates established management strategies such as aspirin and heparin, and explores adjunctive or investigational therapies, including hydroxychloroquine, corticosteroids, intravenous immunoglobulins, statins, plasma exchange, and biologics. Key knowledge gaps, concerning refractory cases and personalized treatment approaches, are highlighted, emphasizing the importance of multidisciplinary, risk-based care throughout preconception, pregnancy, and postpartum. This review focuses primarily on primary OAPS rather than secondary APS associated with systemic lupus erythematosus.</p><p><strong>Expert opinion: </strong>Innovations in immunotherapy and targeted biologics hold promise for refractory OAPS; however, large trials are needed to confirm their safety and efficacy during pregnancy. Future management is likely to involve biomarker-driven strategies, incorporating machine learning to enhance prediction and individualization of treatment. The development of standardized diagnostic criteria and risk assessment tools, alongside multidisciplinary collaboration, will be crucial in advancing care, ultimately transforming maternal-fetal health outcomes.</p>","PeriodicalId":12175,"journal":{"name":"Expert Review of Clinical Immunology","volume":" ","pages":"1-12"},"PeriodicalIF":3.7,"publicationDate":"2026-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}