Pub Date : 2025-08-19DOI: 10.1016/j.coi.2025.102645
Kimberly A Thomas , Rachael P Jackman
The rising interest in using cold-stored platelets (CSP) for improving outcomes in patients with active bleeding has led to multiple clinical trials with the goal of determining the in vivo hemostatic efficacy of CSP compared to standard-of-care room temperature–stored platelets. These trials are concentrated predominantly on safety and hemostatic efficacy measurements in response to therapeutic transfusion with CSP, with safety focused on the usual immune-mediated adverse reactions associated with transfusion, such as allergic and alloimmune reactions. However, given the established relationship between thrombosis and inflammation/immune activation as seen in atherosclerosis, autoimmune disease, and infection (to include the recent COVID-19 pandemic), the goal of this review is to highlight additional mechanisms by which CSP may potentiate or dampen immune activity in the context of therapeutic CSP transfusion in actively bleeding patients, thus highlighting areas of future research.
{"title":"Potential immune consequences of cold-stored platelet transfusion","authors":"Kimberly A Thomas , Rachael P Jackman","doi":"10.1016/j.coi.2025.102645","DOIUrl":"10.1016/j.coi.2025.102645","url":null,"abstract":"<div><div>The rising interest in using cold-stored platelets (CSP) for improving outcomes in patients with active bleeding has led to multiple clinical trials with the goal of determining the <em>in vivo</em> hemostatic efficacy of CSP compared to standard-of-care room temperature–stored platelets. These trials are concentrated predominantly on safety and hemostatic efficacy measurements in response to therapeutic transfusion with CSP, with safety focused on the usual immune-mediated adverse reactions associated with transfusion, such as allergic and alloimmune reactions. However, given the established relationship between thrombosis and inflammation/immune activation as seen in atherosclerosis, autoimmune disease, and infection (to include the recent COVID-19 pandemic), the goal of this review is to highlight additional mechanisms by which CSP may potentiate or dampen immune activity in the context of therapeutic CSP transfusion in actively bleeding patients, thus highlighting areas of future research.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"96 ","pages":"Article 102645"},"PeriodicalIF":5.8,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144866545","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}
Pub Date : 2025-08-18DOI: 10.1016/j.coi.2025.102642
Giannini Olivier , Elzi Luigia
Patients with chronic kidney disease (CKD), especially those with end-stage kidney disease on dialysis or kidney transplant recipients (KTRs), are highly susceptible to infections, including the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The COVID-19 pandemic disproportionately affected this vulnerable population, leading to increased morbidity and mortality. Immune dysfunction in CKD patients contributes to a suboptimal defense against infections and a reduced response to SARS-CoV-2 vaccinations. Although vaccination has significantly reduced severe outcomes, dialysis patients and KTRs exhibit lower seroconversion rates and faster antibody waning compared to the general population. Recent evidence suggests that booster doses improve immune responses, but vaccine efficacy remains lower in immunosuppressed individuals. This review highlights the epidemiology of COVID-19 in nephropathic patients, the mechanisms underlying their immune dysregulation, and the effectiveness of vaccination strategies. Future directions include optimizing booster regimens, integrating serological and avidity testing to tailor vaccination strategies, and exploring novel immunotherapeutic approaches. A multidisciplinary effort involving nephrologists, immunologists, and public health experts is essential to improve pandemic preparedness and develop targeted strategies to protect nephropathic patients from future viral threats.
{"title":"SARS-CoV-2 and chronic kidney disease: challenges and future directions","authors":"Giannini Olivier , Elzi Luigia","doi":"10.1016/j.coi.2025.102642","DOIUrl":"10.1016/j.coi.2025.102642","url":null,"abstract":"<div><div>Patients with chronic kidney disease (CKD), especially those with end-stage kidney disease on dialysis or kidney transplant recipients (KTRs), are highly susceptible to infections, including the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The COVID-19 pandemic disproportionately affected this vulnerable population, leading to increased morbidity and mortality. Immune dysfunction in CKD patients contributes to a suboptimal defense against infections and a reduced response to SARS-CoV-2 vaccinations. Although vaccination has significantly reduced severe outcomes, dialysis patients and KTRs exhibit lower seroconversion rates and faster antibody waning compared to the general population. Recent evidence suggests that booster doses improve immune responses, but vaccine efficacy remains lower in immunosuppressed individuals. This review highlights the epidemiology of COVID-19 in nephropathic patients, the mechanisms underlying their immune dysregulation, and the effectiveness of vaccination strategies. Future directions include optimizing booster regimens, integrating serological and avidity testing to tailor vaccination strategies, and exploring novel immunotherapeutic approaches. A multidisciplinary effort involving nephrologists, immunologists, and public health experts is essential to improve pandemic preparedness and develop targeted strategies to protect nephropathic patients from future viral threats.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"96 ","pages":"Article 102642"},"PeriodicalIF":5.8,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144866546","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}
Pub Date : 2025-08-18DOI: 10.1016/j.coi.2025.102641
Angel Ray Baroz , Debra K Lee , Natalia Maverakis Ramirez , Smriti K Raychaudhuri , Siba P Raychaudhuri
Psoriasis and psoriatic arthritis are chronic autoimmune diseases characterized by dysregulated immune responses, particularly involving Th17 cells. Immune checkpoint molecules such as programmed death-1 (PD-1) and its ligands (PD-L1/PD-L2) are critical for maintaining immune tolerance. Disruptions in these pathways contribute to psoriatic disease pathogenesis. Notably, immune checkpoint inhibitors used in cancer therapy have been linked to the development of psoriasis or its exacerbation. This highlights the complex role of checkpoint pathways in psoriatic diseases. Thus, immune checkpoint agonists could be a therapeutic strategy aimed at restoring immune balance without widespread immunosuppression. Preclinical studies demonstrate that PD-1 agonists can mitigate inflammation by enhancing inhibitory signaling. Additionally, early-phase clinical trials in autoimmune diseases such as rheumatoid arthritis and ulcerative colitis suggest potential benefits of PD-1 modulation in psoriasis. This review explores immune checkpoint agonists in psoriatic disease as a promising alternative to conventional immunosuppressants by selectively suppressing pathogenic T-cell activity.
{"title":"Checkpoint agonists — immunoregulatory role and its implications in the treatment of psoriasis and psoriatic arthritis","authors":"Angel Ray Baroz , Debra K Lee , Natalia Maverakis Ramirez , Smriti K Raychaudhuri , Siba P Raychaudhuri","doi":"10.1016/j.coi.2025.102641","DOIUrl":"10.1016/j.coi.2025.102641","url":null,"abstract":"<div><div>Psoriasis and psoriatic arthritis are chronic autoimmune diseases characterized by dysregulated immune responses, particularly involving Th17 cells. Immune checkpoint molecules such as programmed death-1 (PD-1) and its ligands (PD-L1/PD-L2) are critical for maintaining immune tolerance. Disruptions in these pathways contribute to psoriatic disease pathogenesis. Notably, immune checkpoint inhibitors used in cancer therapy have been linked to the development of psoriasis or its exacerbation. This highlights the complex role of checkpoint pathways in psoriatic diseases. Thus, immune checkpoint agonists could be a therapeutic strategy aimed at restoring immune balance without widespread immunosuppression. Preclinical studies demonstrate that PD-1 agonists can mitigate inflammation by enhancing inhibitory signaling. Additionally, early-phase clinical trials in autoimmune diseases such as rheumatoid arthritis and ulcerative colitis suggest potential benefits of PD-1 modulation in psoriasis. This review explores immune checkpoint agonists in psoriatic disease as a promising alternative to conventional immunosuppressants by selectively suppressing pathogenic T-cell activity.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"96 ","pages":"Article 102641"},"PeriodicalIF":5.8,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144860382","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}
Pub Date : 2025-08-14DOI: 10.1016/j.coi.2025.102636
Jingyi Tang, Erle Dang, Gang Wang
Psoriasis is a chronic autoimmune skin disease characterized by abnormal proliferation and differentiation of keratinocytes, with a complex pathogenesis often linked to environmental and genetic factors. Although many treatments are available, the disease still exhibits a high recurrence rate. Epigenetic regulation appears to bridge external stimuli and genetic abnormalities in the development of psoriasis. Skin-resident cells may contribute to disease recurrence through an ‘inflammatory memory’ formed through epigenetic modifications. This review focuses on skin-resident cells in psoriasis, elucidating their roles in disease progression and recurrence from an epigenetic perspective, providing scientific evidence for targeted therapies.
{"title":"Implication of epigenetic factors in development and recurrence of psoriasis","authors":"Jingyi Tang, Erle Dang, Gang Wang","doi":"10.1016/j.coi.2025.102636","DOIUrl":"10.1016/j.coi.2025.102636","url":null,"abstract":"<div><div>Psoriasis is a chronic autoimmune skin disease characterized by abnormal proliferation and differentiation of keratinocytes, with a complex pathogenesis often linked to environmental and genetic factors. Although many treatments are available, the disease still exhibits a high recurrence rate. Epigenetic regulation appears to bridge external stimuli and genetic abnormalities in the development of psoriasis. Skin-resident cells may contribute to disease recurrence through an ‘inflammatory memory’ formed through epigenetic modifications. This review focuses on skin-resident cells in psoriasis, elucidating their roles in disease progression and recurrence from an epigenetic perspective, providing scientific evidence for targeted therapies.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"96 ","pages":"Article 102636"},"PeriodicalIF":5.8,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144829092","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}
Pub Date : 2025-08-14DOI: 10.1016/j.coi.2025.102640
Tessa L Clement, Philip L Cohen
A general understanding of the mechanisms leading to the development of systemic lupus has emerged over recent years, yet treatment of the illness remains largely empiric and unsatisfactory. Targeted therapy with monoclonal antibodies directed against B cells and against cytokines has met limited success, as has therapy with mesenchymal and hematopoietic stem cells. In the last few years, treatment of refractory disease with chimeric-antigen reactive T cells directed against B cells (CAR-T cells) has shown unexpected promise in small patient series, with apparent long-term and complete remission of disease. Rapid progress in this area is likely to result in improved T cell and natural killer (NK) cell treatment of patients with more readily accessible and practical methods. In parallel, increased understanding of systemic lupus erythematosus disease mechanisms using systems biology and single-cell approaches is likely to uncover additional pathways to intervene in the pathogenesis of disease, raising hopes that additional options will be available for long-term treatment or cure of the disease or even prevention of disease in susceptible individuals.
{"title":"Can we cure lupus?","authors":"Tessa L Clement, Philip L Cohen","doi":"10.1016/j.coi.2025.102640","DOIUrl":"10.1016/j.coi.2025.102640","url":null,"abstract":"<div><div>A general understanding of the mechanisms leading to the development of systemic lupus has emerged over recent years, yet treatment of the illness remains largely empiric and unsatisfactory. Targeted therapy with monoclonal antibodies directed against B cells and against cytokines has met limited success, as has therapy with mesenchymal and hematopoietic stem cells. In the last few years, treatment of refractory disease with chimeric-antigen reactive T cells directed against B cells (CAR-T cells) has shown unexpected promise in small patient series, with apparent long-term and complete remission of disease. Rapid progress in this area is likely to result in improved T cell and natural killer (NK) cell treatment of patients with more readily accessible and practical methods. In parallel, increased understanding of systemic lupus erythematosus disease mechanisms using systems biology and single-cell approaches is likely to uncover additional pathways to intervene in the pathogenesis of disease, raising hopes that additional options will be available for long-term treatment or cure of the disease or even prevention of disease in susceptible individuals.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"96 ","pages":"Article 102640"},"PeriodicalIF":5.8,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842745","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}
Pub Date : 2025-08-14DOI: 10.1016/j.coi.2025.102643
Zhi Hu , Ming Zhao
Autoimmune skin diseases (AISDs) constitute a group of skin disorders driven by B cell–mediated autoimmunity or dysregulation of other immune cell populations. AISD can be further divided into systemic autoimmune disease with skin involvement, such as systemic lupus erythematosus (SLE), and skin-specific autoimmune disease, such as pemphigus vulgaris (PV). Due to autoreactivity, B cells and autoantibody production play a pivotal role in B cell–driven AISDs. B cell–targeted therapies have become a major focus in research and clinical practice. Recent strategies targeting various B cell have shown promise, whereas several challenges remain in the clinical application. Patient heterogeneity results in variable therapeutic outcomes. Additionally, prolonged B cell suppression increases the risk of infections. Here, this review outlines the B cell–targeted therapeutic approaches in AISDs, explore the implications of their variable efficacy, and discuss future directions for development. We aim to provide broader perspectives for advancing targeted therapies in AISDs.
{"title":"B cell–targeted therapies in autoimmune skin disease: current advances and challenges","authors":"Zhi Hu , Ming Zhao","doi":"10.1016/j.coi.2025.102643","DOIUrl":"10.1016/j.coi.2025.102643","url":null,"abstract":"<div><div>Autoimmune skin diseases (AISDs) constitute a group of skin disorders driven by B cell–mediated autoimmunity or dysregulation of other immune cell populations. AISD can be further divided into systemic autoimmune disease with skin involvement, such as systemic lupus erythematosus (SLE), and skin-specific autoimmune disease, such as pemphigus vulgaris (PV). Due to autoreactivity, B cells and autoantibody production play a pivotal role in B cell–driven AISDs. B cell–targeted therapies have become a major focus in research and clinical practice. Recent strategies targeting various B cell have shown promise, whereas several challenges remain in the clinical application. Patient heterogeneity results in variable therapeutic outcomes. Additionally, prolonged B cell suppression increases the risk of infections. Here, this review outlines the B cell–targeted therapeutic approaches in AISDs, explore the implications of their variable efficacy, and discuss future directions for development. We aim to provide broader perspectives for advancing targeted therapies in AISDs.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"96 ","pages":"Article 102643"},"PeriodicalIF":5.8,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842746","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}
Pub Date : 2025-08-11DOI: 10.1016/j.coi.2025.102632
Shwetha Maharaj, Christopher Chang
Juvenile idiopathic arthritis (JIA) is the most common rheumatological disorder affecting children. It is characterized by chronic synovial inflammation that may lead to permanent joint damage and disability. JIA is an umbrella term for a heterogenous group of subtypes based on specific clinical and serological features. Each subtype has a multifactorial pathogenesis that involves a complex interplay of genetic susceptibility, environmental triggers, and immune dysregulation. Recent advancements in genomic and multi-omics research have elucidated key genetic and epigenetic contributors to JIA, including risk loci within the highly polymorphic human leukocyte antigen region and monogenic mutations in genes, such as LACC1, UNC13D, and NFIL3. Genome-wide association studies have further revealed that many JIA-associated single-nucleotide polymorphisms (SNPs) reside in noncoding regulatory regions, underscoring the significance of chromatin architecture and transcriptional control in disease development.
While current therapies — including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), biologics, and corticosteroids — offer symptomatic relief, they do not provide a cure, and many patients experience variable treatment responses or adverse effects. Emerging strategies focus on precision medicine approaches, integrating therapeutic biomarkers to predict disease course and optimize treatment. Furthermore, gene therapy using viral and mRNA-based vectors and advanced cell-based therapies — including regulatory T cells (Tregs), CAR-Tregs, and chimeric autoantibody receptor (CAAR)-T cells — are being explored as potential disease-modifying interventions. These innovative approaches aim to restore immune tolerance, reprogram dysregulated immune pathways, and minimize systemic immunosuppression. Although still in experimental stages, these technologies hold promise for achieving durable remission or potential cure in JIA. Continued translational research and clinical trials will be pivotal in realizing the therapeutic potential of these novel interventions.
{"title":"Can juvenile idiopathic arthritis be cured?","authors":"Shwetha Maharaj, Christopher Chang","doi":"10.1016/j.coi.2025.102632","DOIUrl":"10.1016/j.coi.2025.102632","url":null,"abstract":"<div><div>Juvenile idiopathic arthritis (JIA) is the most common rheumatological disorder affecting children. It is characterized by chronic synovial inflammation that may lead to permanent joint damage and disability. JIA is an umbrella term for a heterogenous group of subtypes based on specific clinical and serological features. Each subtype has a multifactorial pathogenesis that involves a complex interplay of genetic susceptibility, environmental triggers, and immune dysregulation. Recent advancements in genomic and multi-omics research have elucidated key genetic and epigenetic contributors to JIA, including risk loci within the highly polymorphic human leukocyte antigen region and monogenic mutations in genes, such as LACC1, UNC13D, and NFIL3. Genome-wide association studies have further revealed that many JIA-associated single-nucleotide polymorphisms (SNPs) reside in noncoding regulatory regions, underscoring the significance of chromatin architecture and transcriptional control in disease development.</div><div>While current therapies — including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), biologics, and corticosteroids — offer symptomatic relief, they do not provide a cure, and many patients experience variable treatment responses or adverse effects. Emerging strategies focus on precision medicine approaches, integrating therapeutic biomarkers to predict disease course and optimize treatment. Furthermore, gene therapy using viral and mRNA-based vectors and advanced cell-based therapies — including regulatory T cells (Tregs), CAR-Tregs, and chimeric autoantibody receptor (CAAR)-T cells — are being explored as potential disease-modifying interventions. These innovative approaches aim to restore immune tolerance, reprogram dysregulated immune pathways, and minimize systemic immunosuppression. Although still in experimental stages, these technologies hold promise for achieving durable remission or potential cure in JIA. Continued translational research and clinical trials will be pivotal in realizing the therapeutic potential of these novel interventions.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"96 ","pages":"Article 102632"},"PeriodicalIF":5.8,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144828039","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}
Antiphospholipid syndrome (APS) is an acquired autoimmune thrombophilia. Complement system, which shares common actors with the coagulation cascade, is nowadays well established to be implicated in APS pathophysiology by different mechanisms. In APS, complement activation assessment is not included in the routine care despite numerous studies showing the presence of activation fragments (C4d, C3d, and C5b9) at a systemic level in sera and blood cells’ surface but also in affected arterial walls, kidneys, placentas, or heart valves. APS patients are treated to prevent thrombosis recurrence by long-term anticoagulation with vitamin K antagonist. Several case reports described the use of an anti-C5 antibody to treat particular forms of APS (recurrent thrombosis, catastrophic APS) but are not sufficient to conclude on its efficacy. There is still a need to identify relevant biomarkers to help establish the role of the various recently developed complement-targeting molecules in the therapeutic approach to APS.
{"title":"Complement in antiphospholipid syndrome, time to target?","authors":"Marie-Agnès Dragon Durey , Houcine Hamidi , Luc Darnige","doi":"10.1016/j.coi.2025.102628","DOIUrl":"10.1016/j.coi.2025.102628","url":null,"abstract":"<div><div>Antiphospholipid syndrome (APS) is an acquired autoimmune thrombophilia. Complement system, which shares common actors with the coagulation cascade, is nowadays well established to be implicated in APS pathophysiology by different mechanisms. In APS, complement activation assessment is not included in the routine care despite numerous studies showing the presence of activation fragments (C4d, C3d, and C5b9) at a systemic level in sera and blood cells’ surface but also in affected arterial walls, kidneys, placentas, or heart valves. APS patients are treated to prevent thrombosis recurrence by long-term anticoagulation with vitamin K antagonist. Several case reports described the use of an anti-C5 antibody to treat particular forms of APS (recurrent thrombosis, catastrophic APS) but are not sufficient to conclude on its efficacy. There is still a need to identify relevant biomarkers to help establish the role of the various recently developed complement-targeting molecules in the therapeutic approach to APS.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"96 ","pages":"Article 102628"},"PeriodicalIF":5.8,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144779523","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}
Pub Date : 2025-08-06DOI: 10.1016/j.coi.2025.102629
Valentin Baverel , Carmen Garrido , Evelyne Kohli
Macrophages and the complement system are fundamental components of innate immunity, emerging early in evolutionary history. The well-established functions of complement in relation to macrophages contribute to both innate and adaptive immunity and are mediated by extracellular components acting systemically or locally within tissues.
A novel compartment, termed intracellular complement or the ‘complosome’, was first identified in 2013 within CD4+ T cells, marking the onset of an active research field. Intracellular complement has been associated with responses to both infectious and noninfectious stimuli, akin to extracellular complement, while also exhibiting significant autocrine functions in cell metabolism and homeostasis.
This review focuses on intracellular complement within monocytes/macrophages. After a brief overview of the complement system and its canonical roles in these cells, we define intracellular complement and discuss current knowledge regarding its expression and functions in monocytes/macrophages, as well as its potential links to human diseases.
{"title":"Intracellular complement in monocytes and macrophages: emerging roles","authors":"Valentin Baverel , Carmen Garrido , Evelyne Kohli","doi":"10.1016/j.coi.2025.102629","DOIUrl":"10.1016/j.coi.2025.102629","url":null,"abstract":"<div><div>Macrophages and the complement system are fundamental components of innate immunity, emerging early in evolutionary history. The well-established functions of complement in relation to macrophages contribute to both innate and adaptive immunity and are mediated by extracellular components acting systemically or locally within tissues.</div><div>A novel compartment, termed intracellular complement or the ‘complosome’, was first identified in 2013 within CD4+ T cells, marking the onset of an active research field. Intracellular complement has been associated with responses to both infectious and noninfectious stimuli, akin to extracellular complement, while also exhibiting significant autocrine functions in cell metabolism and homeostasis.</div><div>This review focuses on intracellular complement within monocytes/macrophages. After a brief overview of the complement system and its canonical roles in these cells, we define intracellular complement and discuss current knowledge regarding its expression and functions in monocytes/macrophages, as well as its potential links to human diseases.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"96 ","pages":"Article 102629"},"PeriodicalIF":5.8,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144779524","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}
Pub Date : 2025-08-06DOI: 10.1016/j.coi.2025.102631
James K Sullivan , Audrey Kwun , Trine N Jørgensen
Neuropsychiatric lupus (NPSLE) is believed to manifest in 30–40% of SLE patients, with symptoms spanning from fatigue and anxiety to depression, cognitive impairment, and psychosis. Over the past decades, it has become clear that most animal models of SLE also present with some level of NPSLE-like disease. Similar to the diversity of presentations among NPSLE patients, symptoms of NPSLE differ between animal models, likely due to their fixed genetic background. Therefore, both genetic and therapeutic studies have focused on different mechanisms in different models, making it difficult to translate basic research findings to the clinical realm. Here, we summarize studies of different animal models of NPSLE, specifically focusing on differences and overlaps between identified pathological pathways.
{"title":"Neuropsychiatric lupus: a myriad of symptoms requires a myriad of models","authors":"James K Sullivan , Audrey Kwun , Trine N Jørgensen","doi":"10.1016/j.coi.2025.102631","DOIUrl":"10.1016/j.coi.2025.102631","url":null,"abstract":"<div><div>Neuropsychiatric lupus (NPSLE) is believed to manifest in 30–40% of SLE patients, with symptoms spanning from fatigue and anxiety to depression, cognitive impairment, and psychosis. Over the past decades, it has become clear that most animal models of SLE also present with some level of NPSLE-like disease. Similar to the diversity of presentations among NPSLE patients, symptoms of NPSLE differ between animal models, likely due to their fixed genetic background. Therefore, both genetic and therapeutic studies have focused on different mechanisms in different models, making it difficult to translate basic research findings to the clinical realm. Here, we summarize studies of different animal models of NPSLE, specifically focusing on differences and overlaps between identified pathological pathways.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":"96 ","pages":"Article 102631"},"PeriodicalIF":5.8,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144779613","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}
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