Autoimmunity reviews最新文献

{"title":"Fecal microbiota transplantation in autoimmune diseases – An extensive paper on a pathogenetic therapy","authors":"","doi":"10.1016/j.autrev.2024.103541","DOIUrl":"10.1016/j.autrev.2024.103541","url":null,"abstract":"<div><p>The role of infections in the pathogenesis of autoimmune diseases has long been recognized and reported. In addition to infectious agents, the internal composition of the “friendly” living bacteria, (microbiome) and its correlation to immune balance and dysregulation have drawn the attention of researchers for decades. Nevertheless, only recently, scientific papers regarding the potential role of transferring microbiome from healthy donor subjects to patients with autoimmune diseases has been proposed. Fecal microbiota transplantation or FMT, carries the logic of transferring microorganisms responsible for immune balance from healthy donors to individuals with immune dysregulation or more accurately for our paper, autoimmune diseases. Viewing the microbiome as a pathogenetic player allows us to consider FMT as a pathogenetic-based treatment. Promising results alongside improved outcomes have been demonstrated in patients with different autoimmune diseases following FMT. Therefore, in our current extensive review, we aimed to highlight the implication of FMT in various autoimmune diseases, such as inflammatory bowel disease, autoimmune thyroid and liver diseases, systemic lupus erythematosus, and type 1 diabetes mellitus, among others. Presenting all the aspects of FMT in more than 12 autoimmune diseases in one paper, to the best of our knowledge, is the first time presented in medical literature. Viewing FMT as such could contribute to better understanding and newer application of the model in the therapy of autoimmune diseases, indeed.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 7","pages":"Article 103541"},"PeriodicalIF":9.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140777104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rituximab-induced cystoid macular edema in a patient with systemic lupus erythematosus: A case report and literature review","authors":"Victoria Lobo-Antuña ,&nbsp;Anbar Cherti-Afailal ,&nbsp;Marta García-Morales ,&nbsp;Raquel Ríos-Fernández ,&nbsp;Francisco Javier de la Hera-Fernández ,&nbsp;Jose Luis García-Serrano ,&nbsp;Jose Luis Callejas-Rubio","doi":"10.1016/j.autrev.2024.103588","DOIUrl":"10.1016/j.autrev.2024.103588","url":null,"abstract":"<div><p>Cystoid macular edema (CME) is considered a rare adverse effect of rituximab use, with only a limited number of cases published in the literature. Although its etiopathogenesis is still unknown, its mechanism seems to be related to a transient elevation of cytokines after rituximab infusion resulting in an increased permeability of retinal vessels.</p><p>We report the first case of rituximab-induced CME in a patient with systemic lupus erythematosus (SLE), where rituximab was used to treat hematological complications. A month after the 2nd infusion, the patient developed blurred vision and decreased visual acuity in the right eye. An optic coherence tomography (OCT) was performed, being diagnosed with CME. Rituximab was then discontinued, exhibiting a complete resolution of the condition within 4 weeks. The aim of our work is to report the first case in a patient with SLE and also carry out a brief review of the subject comparing it to all previously published cases.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 7","pages":"Article 103588"},"PeriodicalIF":9.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disease phenotypes in adult patients with suspected undifferentiated autoinflammatory diseases and PFAPA syndrome: Clinical and therapeutic implications","authors":"","doi":"10.1016/j.autrev.2024.103520","DOIUrl":"10.1016/j.autrev.2024.103520","url":null,"abstract":"<div><h3>Background</h3><p>Undifferentiated autoinflammatory diseases are characterized by recurrent or persistent fever, usually combined with other inflammatory manifestations, and negative or inconclusive genetic studies for monogenic autoinflammatory disorders.</p></div><div><h3>Aims</h3><p>To define and characterize disease phenotypes in adult patients diagnosed in an adult reference center with undifferentiated autoinflammatory diseases, and to analyze the efficacy of the drugs used in order to provide practical diagnostic and therapeutic recommendations.</p></div><div><h3>Methods</h3><p>Retrospective study (2015–2022) of patients with undifferentiated autoinflammatory diseases among all patients visited in our reference center. Demographic, clinical, laboratory features and detailed therapeutic information was collected.</p></div><div><h3>Results</h3><p>Of the 334 patients with a suspected autoinflammatory disease, 134 (40%) patients (61% women) were initially diagnosed with undifferentiated autoinflammatory diseases. Mean age at disease onset and at diagnosis was 28.7 and 37.7 years, respectively. In 90 (67.2%) patients, symptoms started during adulthood. Forty-four (32.8%) patients met diagnostic/classification criteria for adult periodic fever with aphthous stomatitis, pharyngitis and cervical adenitis (PFAPA) syndrome. In the remaining patients, four additional phenotypes were differentiated according to the predominant manifestations: a) Predominantly fever phenotype (<em>n</em> = 18; 13.4%); b) Predominantly abdominal/pleuritic pain phenotype (<em>n</em> = 9; 6.7%); c) Predominantly pericarditis phenotype (n = 18; 13.4%), and d) Complex syndrome phenotype (<em>n</em> = 45; 33.6%). Prednisone (mainly on demand), colchicine and anakinra were the drugs commonly used. Overall, complete responses were achieved with prednisone in 41.3%, colchicine in 40.2%, and anakinra in 58.3% of patients in whom they were used. By phenotypes, prednisone on demand was more effective in adult PFAPA syndrome and colchicine in patients with the abdominal/pleuritic pain pattern and PFAPA syndrome. Patients with complex syndrome achieved complete responses with prednisone (21.9%), colchicine (25.7%) and anakinra (44.4%), and were the group more often requiring additional immunosuppressive drugs.</p></div><div><h3>Conclusions</h3><p>The analysis of the largest single-center series of adult patients with undifferentiated autoinflammatory diseases identified and characterized different disease phenotypes and their therapeutic approaches. This study is expected to contribute to increase the awareness of physicians for an early identification of these conditions, and to provide the best known therapeutic options.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 7","pages":"Article 103520"},"PeriodicalIF":9.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1568997224000077/pdfft?md5=fc590fae74c4fd13c9b544cd7993f7f9&pid=1-s2.0-S1568997224000077-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological markers of high risk of thrombotic recurrence in patients with antiphospholipid syndrome: A literature review","authors":"Mathilde Lambert ,&nbsp;Alexandre Brodovitch ,&nbsp;Jean-Louis Mège ,&nbsp;Daniel Bertin ,&nbsp;Nathalie Bardin","doi":"10.1016/j.autrev.2024.103585","DOIUrl":"10.1016/j.autrev.2024.103585","url":null,"abstract":"<div><h3>Objectives</h3><p>This review aims to identify biological markers associated with the risk of recurrence of thrombotic and/or obstetric events in patients with antiphospholipid syndrome (APS).</p></div><div><h3>Methods</h3><p>A comprehensive review of literature was conducted to evaluate established and potential novel biological markers associated with thrombosis in APS. To this end, a PubMed literature search was conducted for the last twenty years using the following keywords or their combinations: thrombotic risk, recurrence of thrombosis, risk stratification, severity, predictive value.</p></div><div><h3>Results</h3><p>Previous studies showed that multiple aPL positivity correlates with an increased risk of thrombosis in APS. Moreover, the analysis of N-glycosylation of antiphospholipid antibodies (aPL) revealed that low levels of IgG sialylation, fucosylation or galactosylation increases the pro-inflammatory activity of aPL, predisposing to thrombosis. In addition, quantification of neutrophil extracellular traps (NETs) and antibodies directed against NETs (anti-NETs) in serum demonstrates promising prognostic utility in assessing APS severity. Oxidative stress plays a role in the pathogenicity of APS and paraoxonase 1 (PON1) activity emerges as a promising biomarker of thrombotic risk in APS. Furthermore, identification of novel antigenic targets involved in the pathophysiology of APS, such as lysobisphosphatidic acid (LBPA), had led to the discovery of unconventional aPL, antibodies directed against the LBPA (aLBPA), whose clinical value could make it possible to identify APS patients at high risk of thrombotic recurrence.</p></div><div><h3>Conclusion</h3><p>The immunological profile of aPL, N-glycosylation of aPL, quantification of NETs and anti-NETs, analysis of biomarkers of oxidative stress and the discovery of aLBPA offer potential prognostic tools for risk stratification in APS patients.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 6","pages":"Article 103585"},"PeriodicalIF":9.2,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1568997224000764/pdfft?md5=7fea2f78a470f8e3326f85a6a27f3e34&pid=1-s2.0-S1568997224000764-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141878298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposome: Epigenetics and autoimmune diseases","authors":"Maria Giovanna Danieli ,&nbsp;Marco Casciaro ,&nbsp;Alberto Paladini ,&nbsp;Martina Bartolucci ,&nbsp;Martina Sordoni ,&nbsp;Yehuda Shoenfeld ,&nbsp;Sebastiano Gangemi","doi":"10.1016/j.autrev.2024.103584","DOIUrl":"10.1016/j.autrev.2024.103584","url":null,"abstract":"<div><p>Systemic autoimmune diseases are complex conditions characterized by an immune system dysregulation and an aberrant activation against self-antigens, leading to tissue and organ damage. Even though genetic predisposition plays a role, it cannot fully explain the onset of these diseases, highlighting the significant impact of non-heritable influences such as environment, hormones and infections. The exposome represents all those factors, ranging from chemical pollutants and dietary components to psychological stressors and infectious agents.</p><p>Epigenetics, which studies changes in gene expression without altering the DNA sequence, is a crucial link between exposome and the development of autoimmune diseases. Key epigenetic mechanisms include DNA methylation, histone modifications, and non-coding RNAs.</p><p>These epigenetic modifications could provide a potential piece of the puzzle in understanding systemic autoimmune diseases and their connection with the exposome.</p><p>In this work we have collected the most important and recent evidence in epigenetic changes linked to systemic autoimmune diseases (systemic lupus erythematosus, idiopathic inflammatory myopathies, ANCA-associated vasculitis, and rheumatoid arthritis), emphasizing the roles these changes may play in disease pathogenesis, their potential as diagnostic biomarkers and their prospective in the development of targeted therapies.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 6","pages":"Article 103584"},"PeriodicalIF":9.2,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1568997224000752/pdfft?md5=086de9b170a469a777780c8148af52a0&pid=1-s2.0-S1568997224000752-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular and cerebrovascular outcomes in anti-neutrophil cytoplasmic antibody-associated vasculitis: A systematic review with meta-analysis","authors":"Wenhui Xie ,&nbsp;Shiyu Xiao ,&nbsp;Xiaoyuan Li ,&nbsp;Jing Huang ,&nbsp;Zhuoli Zhang","doi":"10.1016/j.autrev.2024.103587","DOIUrl":"10.1016/j.autrev.2024.103587","url":null,"abstract":"<div><h3>Objective</h3><p>To quantify the magnitude of the risk of total and type-specific cardiovascular and cerebrovascular diseases (CCVD) in patients with anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV).</p></div><div><h3>Method</h3><p>Searches of PubMed, Embase, and the Cochrane Library were conducted. Observational studies were included if they reported data on CCVD in AAV patients. Pooled risk ratios (RR) with 95% confidence intervals were calculated.</p></div><div><h3>Result</h3><p>Fourteen studies met the inclusion criteria, comprising 20,096 AAV patients (over 46,495 person-years) with 5757 CCVD events. Compared with non-vasculitis population, AAV patients showed an 83% increased risk of incident CCVD (1.83 [1.37–2.45]; <em>n</em> = 10), 48% for coronary artery disease (1.48 [1.26–1.75]; <em>n</em> = 9), and 56% for cerebrovascular accident (1.56 [1.22–1.99]; n = 9). For type-specific CCVD, the risks of myocardial infarction, stroke, heart failure were increased by 67% (1.67 [1.29–2.15]; <em>n</em> = 6), 97% (1.97 [1.19–3.25]; <em>n</em> = 8) and 72% (1.72 [1.28–2.32]; <em>n</em> = 4), whereas there was only a trend toward a higher risk of angina pectoris (1.46 [0.90–2.39]; <em>n</em> = 2), and ischemic stroke (1.88 [0.86–4.12]; n = 4). Subgroup analyses by AAV type found significantly increased CCVD risk in both granulomatosis with polyangiitis (1.87 [1.29–2.73]; <em>n</em> = 7) and microscopic polyangiitis (2.93 [1.58–5.43]; <em>n</em> = 3). In three studies reporting impact of follow-up period after AAV diagnosis, the CCVD risk was significantly higher in the first two years after diagnosis than the subsequent follow-up (2.23 [2.00–2.48] vs. 1.48 [1.40–1.56]; <em>p</em> &lt; 0.01). Significant heterogeneity existed in the main analyses.</p></div><div><h3>Conclusion</h3><p>This meta-analysis demonstrates that AAV is associated with increased risks of overall and type-specific CCVD, especially within two years after AAV diagnosis.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 6","pages":"Article 103587"},"PeriodicalIF":9.2,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relapses in giant cell arteritis: Updated review for clinical practice","authors":"Marco A. Alba ,&nbsp;Tanaz A. Kermani ,&nbsp;Sebastian Unizony ,&nbsp;Giuseppe Murgia ,&nbsp;Sergio Prieto-González ,&nbsp;Carlo Salvarani ,&nbsp;Eric L. Matteson","doi":"10.1016/j.autrev.2024.103580","DOIUrl":"10.1016/j.autrev.2024.103580","url":null,"abstract":"<div><p>Giant cell arteritis (GCA), the most common primary vasculitis in adults, is a granulomatous systemic vasculitis usually affecting the aorta and its major branches, particularly the carotid and vertebral arteries. Although remission can be achieved in most patients with GCA using high-dose glucocorticoids (GC), relapses are frequent, occurring in &gt;40% of GC-only treated patients, mostly during the first two years after diagnosis. Relapsing courses lead to high GC exposure, increasing the risk of treatment-related adverse effects. Although tocilizumab is an efficacious GC-sparing therapy that allows increased sustained remission and reduced cumulative GC doses, relapses are common after drug discontinuation.</p><p>This narrative review examines the most relevant features of relapses in GCA, including its definition, classification, frequency, clinical, laboratory, and imaging characteristics, chronology, probable pathophysiology, and predictive factors. In addition, we discuss treatment options for relapsing patients and the effect of relapses on patient outcomes.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 6","pages":"Article 103580"},"PeriodicalIF":9.2,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Practical guidance for the early recognition and follow-up of patients with connective tissue disease-related interstitial lung disease","authors":"Julien Guiot ,&nbsp;Jelle Miedema ,&nbsp;Ana Cordeiro ,&nbsp;Jeska K. De Vries-Bouwstra ,&nbsp;Theodoros Dimitroulas ,&nbsp;Klaus Søndergaard ,&nbsp;Argyrios Tzouvelekis ,&nbsp;Vanessa Smith","doi":"10.1016/j.autrev.2024.103582","DOIUrl":"10.1016/j.autrev.2024.103582","url":null,"abstract":"<div><h3>Background</h3><p>The early detection and management of (progressive) interstitial lung disease in patients with connective tissue diseases requires the attention and skills of a multidisciplinary team. However, there are currently no well-established standards to guide the daily practice of physicians treating this heterogenous group of diseases.</p></div><div><h3>Research question</h3><p>This paper aimed to identify gaps in scientific knowledge along the journey of patients with connective tissue disease-related interstitial lung disease and to provide tools for earlier identification of interstitial lung disease and progressive disease.</p></div><div><h3>Study Design and Methods</h3><p>The opinions of an international expert panel, which consisted of pulmonologists and rheumatologists were collected and interpreted in the light of peer-reviewed data.</p></div><div><h3>Results</h3><p>Interstitial lung disease is a common complication of connective tissue diseases, but prevalence estimates vary by subtype. Screening and monitoring by means of clinical examination, chest radiography, pulmonary function testing, and disease-specific biomarkers provide insight into the disease activity of patients presenting with connective tissue diseases in a routine setting. Multiple phenotypic and genotypic characteristics have been identified as predictors of the development and progression of interstitial lung disease. However, these risk factors differ between subtypes. To ensure earlier diagnosis of rapidly progressive phenotypes, a risk-based method is necessary for determining the need for HRCT and additional testing.</p></div><div><h3>Interpretation</h3><p>To reduce the underdiagnosis of CTD-ILDs in clinical practice, a standardized and systematic multidisciplinary risk-based approach is suggested. Collaboration across disciplines is essential for the management of CTD-ILD.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 6","pages":"Article 103582"},"PeriodicalIF":9.2,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141791721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the global burden of inflammatory bowel disease (1990–2019): A Joinpoint regression analysis of divergent trends in 10–24 and 50–69 age cohorts","authors":"Xinyi Wang ,&nbsp;Ruipu Xiu ,&nbsp;Liping Gong ,&nbsp;Wei Sun ,&nbsp;Yuxin Dong ,&nbsp;Weitong Liu ,&nbsp;Xiaoxuan Liu ,&nbsp;Chuanyong Liu ,&nbsp;Jingxin Li ,&nbsp;Yanqing Wang","doi":"10.1016/j.autrev.2024.103586","DOIUrl":"10.1016/j.autrev.2024.103586","url":null,"abstract":"<div><h3>Background and aims</h3><p>The escalating prevalence of IBD within specific age cohorts, 10–24 and 50–69 years, necessitates a refined understanding of its epidemiological patterns. Prior investigations have often been constrained by their limited scope, particularly in employing age-specific analyses and utilizing advanced statistical methods such as joinpoint regression. Our research examines these demographic segments to elucidate the epidemiological trajectory of IBD.</p></div><div><h3>Methods</h3><p>This study analyzed GBD 2019 data on IBD, focusing on age groups 10–24 and 50–69. We integrated the socio-demographic index for socio-economic context and employed joinpoint regression to analyze time-segmented disease trends, prioritizing average annual percent change for a comprehensive view.</p></div><div><h3>Results</h3><p>A notable global decline in IBD incidence, particularly in the 50–69 age group, was observed. The 10–24 cohort, however, presented a marginal rise across three decades, with a discernible decline between 2010 and 2019. The study also revealed pivotal gender disparities, with increasing incidence rates in males, especially in the High-income Asia Pacific region. Conversely, females demonstrated decreasing trends across the board. Regional variations accentuated East Asia's escalated IBD incidence and prevalence, whereas high-income North American and Asia-Pacific regions, along with Europe, reflected the highest age-standardized incidence rates.</p></div><div><h3>Conclusion</h3><p>The burden of IBD between 1990 and 2019 presents notable disparities across different regions and age demographics. While older populations are seeing a decrease in IBD incidence, young adults and adolescents in regions like East Asia and high-income Asia Pacific are experiencing a concerning uptick. This uneven distribution, influenced by both age and gender, underscores the multifaceted nature of IBD's global impact.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 6","pages":"Article 103586"},"PeriodicalIF":9.2,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141858855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic heterogeneity in tumor microenvironment – A novel landmark for immunotherapy","authors":"Chen Chen ,&nbsp;Peng Han ,&nbsp;Yanping Qing","doi":"10.1016/j.autrev.2024.103579","DOIUrl":"10.1016/j.autrev.2024.103579","url":null,"abstract":"<div><p>The surrounding non-cancer cells and tumor cells that make up the tumor microenvironment (TME) have various metabolic rhythms. TME metabolic heterogeneity is influenced by the intricate network of metabolic control within and between cells. DNA, protein, transport, and microbial levels are important regulators of TME metabolic homeostasis. The effectiveness of immunotherapy is also closely correlated with alterations in TME metabolism. The response of a tumor patient to immunotherapy is influenced by a variety of variables, including intracellular metabolic reprogramming, metabolic interaction between cells, ecological changes within and between tumors, and general dietary preferences. Although immunotherapy and targeted therapy have made great strides, their use in the accurate identification and treatment of tumors still has several limitations. The function of TME metabolic heterogeneity in tumor immunotherapy is summarized in this article. It focuses on how metabolic heterogeneity develops and is regulated as a tumor progresses, the precise molecular mechanisms and potential clinical significance of imbalances in intracellular metabolic homeostasis and intercellular metabolic coupling and interaction, as well as the benefits and drawbacks of targeted metabolism used in conjunction with immunotherapy. This offers insightful knowledge and important implications for individualized tumor patient diagnosis and treatment plans in the future.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 6","pages":"Article 103579"},"PeriodicalIF":9.2,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141615868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}