Clinical Immunology Communications最新文献

{"title":"Clinical associations of cytopenias in inborn errors of immunity in the USIDNET registry","authors":"Rifat S. Rahman ,&nbsp;Laith M. Haj-Ahmad ,&nbsp;Niraj C. Patel ,&nbsp;Ramsay L. Fuleihan ,&nbsp;Joyce E. Yu ,&nbsp;Manar Abdalgani","doi":"10.1016/j.clicom.2026.01.005","DOIUrl":"10.1016/j.clicom.2026.01.005","url":null,"abstract":"<div><h3>Background</h3><div>Cytopenias may be an initial presentation among inborn errors of immunity (IEI), but their frequency and clinical associations have not been characterized.</div></div><div><h3>Methods</h3><div>We evaluated cytopenias, mortality, infections, malignancies, and comorbidities among 3,511 patients in the United States Immunodeficiency Network Registry.</div></div><div><h3>Results</h3><div>Of the 3,511 patients analyzed, 2,087 (59.4 %) were classified as having antibody deficiencies. Common variable immunodeficiency was most common (40.3 %). Approximately 27.0 % of patients were reported to have at least one cytopenia with anemia in 15.8 %, thrombocytopenia in 11.1 %, neutropenia in 7.2 %, and lymphopenia in 6.7 %. IEI patients carried a 13.5-fold higher rate of cytopenias as compared to general population. Among cytopenias, 239/947 (25.2 %) were immune-mediated. Cytopenias were associated with mortality, infections, malignancies, and lung disease.</div></div><div><h3>Conclusion</h3><div>This study presents the largest cohort of IEI patients assessed for cytopenias in the US to date, underscoring the need for prompt recognition and evaluation of correlated clinical outcomes.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"9 ","pages":"Pages 59-70"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146188999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary modulation of the gut–immune–brain axis: nutritional immunoepigenomics for immune regulation in autoimmunity, cancer, and infection","authors":"Arpita Mukherjee","doi":"10.1016/j.clicom.2026.01.004","DOIUrl":"10.1016/j.clicom.2026.01.004","url":null,"abstract":"<div><div>The gut microbiota is emerging as a master regulator of immune homeostasis across infections, cancer, and neuroinflammatory disorders. Dietary inputs dynamically shape microbial ecosystems and induce durable epigenetic reprogramming of host immunity a convergence now defined as nutritional immunoepigenomics. This review posits that specific nutrients (e.g., soluble fibers, omega-3 fatty acids, polyphenols) promote anti-inflammatory microbial profiles that generate metabolites such as short-chain fatty acids and tryptophan catabolites. These act as epigenetic modifiers regulating histone marks (H3K27ac, H3K9me3) and DNA methylation in Tregs, Th17 cells, dendritic cells, and microglia thus modulating immune tolerance and neuroimmune surveillance. I further explore how ketogenic diets and intermittent fasting influence microbiota epigenome signaling. Integrating findings from preclinical and human studies, and highlight translational advances in spectroscopy and multi-omics for non-invasive monitoring of diet-induced immunoepigenetic states. This review advocates precision dietary strategies as programmable modulators of the gut–immune–brain axis to enhance immunological resilience and therapeutic potential.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"9 ","pages":"Pages 42-53"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146037923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of diet on gut microbiome composition: Implications for immune-mediated diseases","authors":"Debora Rondinella ,&nbsp;Ernesto Margarita ,&nbsp;Pauline Celine Raoul ,&nbsp;Francesca Sofia Galli ,&nbsp;Andrea Severino ,&nbsp;Serena Porcari ,&nbsp;Maria Cristina Mele ,&nbsp;Antonio Gasbarrini ,&nbsp;Giovanni Cammarota ,&nbsp;Emanuele Rinninella ,&nbsp;Gianluca Ianiro","doi":"10.1016/j.clicom.2025.12.001","DOIUrl":"10.1016/j.clicom.2025.12.001","url":null,"abstract":"<div><div>Diet is a key modulator of the gut microbiome, which in turn regulates immune function and inflammation. Western dietary patterns, characterized by high intake of fat, sugar, and ultra-processed foods, are associated with gut dysbiosis, increased intestinal permeability, reduced short-chain fatty acid (SCFA) production, and heightened systemic inflammation. In contrast, Mediterranean, high-fiber, plant-based, and fermented-food diets promote microbial diversity, enhance SCFA synthesis, improve gut barrier integrity, and support immune tolerance by modulating regulatory T cell activity. These dietary patterns have demonstrated potential to reduce inflammation and improve outcomes in immune-mediated diseases (IMDs). Current evidence highlights the importance of nutrition strategies to restore healthy microbiome balance and mitigate inflammation, though further clinical trials are needed to confirm efficacy and guide clinical application. This review aims to provide evidence of the negative and positive diets along with the therapeutic potentials within the context of IMDs and emphasizes the need for individualized nutrition.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"9 ","pages":"Pages 1-11"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145760839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disease-specific clustering is seen among first-degree relatives in autoimmune rheumatic diseases: A cross-sectional, multi-centre study","authors":"S Chandrashekara ,&nbsp;Padmanabha Shenoy ,&nbsp;Uma Kumar ,&nbsp;Sapan Pandya ,&nbsp;Alakendu Ghosh ,&nbsp;Rajkiran Dudam ,&nbsp;Arghya Chattopadhyay ,&nbsp;Apurva Khare ,&nbsp;Rudra Prosad Goswami ,&nbsp;Banwari Sharma","doi":"10.1016/j.clicom.2026.01.001","DOIUrl":"10.1016/j.clicom.2026.01.001","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to assess the prevalence and pattern of familial autoimmunity and comorbidities among patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and systemic sclerosis (SSc).</div></div><div><h3>Methods</h3><div>This multicentre, cross-sectional study utilized data from the Indian Rheumatology Association database and included patients diagnosed with RA, SLE, or SSc according to ACR/EULAR criteria. Family histories of autoimmune diseases and comorbidities (diabetes, hypertension, and cardiovascular disease) were recorded up to third-degree relatives. Data were analyzed using descriptive statistics, Pearson’s chi-square, and Fisher-Freeman-Halton exact tests.</div></div><div><h3>Results</h3><div>Among 4384 RA, 819 SLE, and 180 SSc patients, valid family history data were available for 3638, 489, and 135 cases, respectively. A positive family history of autoimmune disease was observed in 19.6% of RA, 11.4% of SLE, and 10% of SSc patients (<em>P</em> &lt; 0.001). Familial RA was most common among RA patients (13.3%), whereas SLE-like disease was more frequent among relatives of SLE patients (2.6%). First-degree relatives were predominantly affected (RA 91%, SLE 89.3%, SSc 83.3%). Diabetes (16.7–22.2%) and hypertension (9.5–13.9%) were the most prevalent familial comorbidities, with diabetes showing higher aggregation in SSc families (<em>P</em> = 0.002).</div></div><div><h3>Conclusion</h3><div>Familial autoimmunity is common across major AIRDs, showing strong first-degree aggregation and disease-specific clustering. Distinct familial patterns are observed for autoimmune and metabolic comorbidities. RA demonstrates the strongest immediate familial clustering, whereas SLE displays a broader generational spread.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"9 ","pages":"Pages 23-29"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146037928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systems immunology meets clinical translation: Multi-omic approaches to predict therapy response in cancer and autoimmune disease","authors":"Praveen Kumar Chandra Sekar,&nbsp;Ramakrishnan Veerabathiran","doi":"10.1016/j.clicom.2025.12.002","DOIUrl":"10.1016/j.clicom.2025.12.002","url":null,"abstract":"<div><div>The immune system is governed by complex, interconnected molecular and cellular networks that shape disease risk and treatment outcome. Conventional biomarkers in cancer and autoimmune disease often rely on single parameters and fail to capture immune heterogeneity, resulting in variable therapeutic responses. Systems immunology integrates genomics, transcriptomics, epigenomics, proteomics, metabolomics, and microbiome profiling to generate holistic models of immune function. This review examines how multi-omic integration improves the prediction of therapy response across solid and hematologic malignancies and autoimmune disorders, including rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, and inflammatory bowel disease. Advances in machine learning, network modeling, and spatial biology are discussed as critical enablers of immune stratification and biomarker discovery. Although integrated approaches outperform single-omics predictors, challenges remain in clinical validation, interpretability, and cost-effectiveness. We propose a translational framework in which targeted multi-omic panels and computational modeling guide personalized immunotherapy, shifting immune-based treatment from empirical intervention toward predictive, systems-driven precision medicine.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"9 ","pages":"Pages 12-22"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145884969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disseminated tuberculosis in a pediatric patient with hyper IgE syndrome: A rare case report and review of the literature","authors":"Urooj Khan ,&nbsp;Iqra Khaksar ,&nbsp;Muhammad Maaz Bin Zahid ,&nbsp;Mohsin Hassan ,&nbsp;Noor Ul Haram Khattak ,&nbsp;Nabeel Ahmed","doi":"10.1016/j.clicom.2026.05.003","DOIUrl":"10.1016/j.clicom.2026.05.003","url":null,"abstract":"<div><div>Hyper-IgE Syndrome (HIES), or Job’s Syndrome, is a rare primary immunodeficiency disorder characterised by elevated IgE levels, recurrent skin infections, and pulmonary complications. We report a case of a 9-year-old male with previously confirmed HIES who developed disseminated TB, an unusual but severe complication of this immunodeficiency. The patient presented to the clinic with a persistent cough, fever, respiratory distress, and weight loss. Imaging revealed cavitary lung lesions, hepatosplenomegaly, and lymphadenopathy. Blood and imaging tests confirmed the presence of disseminated TB. Treatment included intravenous antibiotics, anti-tubercular treatment (ATT), and nutritional support. The patient responded well to ATT. This case highlights the rare complications and diagnostic challenges of TB in HIES patients and demonstrates that conventional ATT can be effective even in the setting of significant immunodeficiency. We also conducted an extensive review of the literature and comparison of previously reported cases to ours to gain further insights about the topic.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"9 ","pages":"Pages 147-150"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148177548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anifrolumab in ARF1-related disorder: A case report of clinical response and review of its use in type I interferonopathies","authors":"Tadafumi Yokoyama ,&nbsp;Natsumi Inoue ,&nbsp;Ikue Hata ,&nbsp;Noritaka Oyama ,&nbsp;Naotoshi Sugimoto ,&nbsp;Taizo Wada","doi":"10.1016/j.clicom.2026.05.004","DOIUrl":"10.1016/j.clicom.2026.05.004","url":null,"abstract":"<div><h3>Objective</h3><div>ARF1-related disorder is a rare type I interferonopathy characterized by dysregulated interferon (IFN) signaling and chilblain-like lesions, with no established treatment. We report the clinical and immunological response to anifrolumab (ANI) in a pediatric patient.</div></div><div><h3>Case presentation</h3><div>A 9-year-old girl with a pathogenic ARF1 variant (c.295C&gt;T, p.Arg99Cys) and severe chilblain-like lesions showed markedly elevated type I IFN activity, assessed by IFN-stimulated gene (ISG) score, monocyte CD169 expression, and plasma IFN-α levels. Following ANI initiation, the ISG score decreased within 24 h and normalized within one month. CD169 expression and plasma IFN-α levels also normalized. Clinically, chilblain-like lesions resolved within one month, with sustained remission over 12 months. No serious adverse events were observed.</div></div><div><h3>Conclusion</h3><div>ANI led to rapid clinical improvement and normalization of multiple IFN-related biomarkers, supporting IFNAR1 blockade as a rational targeted therapy for selected patients with ARF1-related disease showing prominent type I IFN pathway activation.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"9 ","pages":"Pages 165-171"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148177547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trends and contemporary epidemiology of mortality with primary immunodeficiency diseases in the United States, 2015–2022","authors":"Ernestina Bioh Hansen-Sackey ,&nbsp;Fredrick Dapaah-Siakwan","doi":"10.1016/j.clicom.2026.01.002","DOIUrl":"10.1016/j.clicom.2026.01.002","url":null,"abstract":"<div><h3>Background</h3><div>There is paucity of data on recent trends of population-level deaths with Primary Immunodeficiency Diseases (PIDD).</div></div><div><h3>Objective</h3><div>To examine the population-based temporal trends in deaths with PIDD in the United States from 2015 to 2022.</div></div><div><h3>Methods</h3><div>We performed a retrospective, serial cross-sectional analysis of national death certificate data from 2015 through 2022. We evaluated the changes in the PIDD age-adjusted mortality rate per 1000,000 (AAMR), overall, then stratified by age, gender, and race/ethnicity.</div></div><div><h3>Results</h3><div>The overall AAMR increased significantly from 2.5 to 3.5 (<em>P</em> &lt; 0.01). The AAMR rose significantly from 2.5 in the pre-COVID-19 era (2015–2019) to 3.2 in the COVID-19 era (2020–2022) [<em>P</em> = 0.03]. A similar trend was seen in several subgroups especially those aged ≥65 years.</div></div><div><h3>Conclusion</h3><div>The overall PIDD AAMR increased during the study period, especially in those aged ≥65 years. This data can enhance PIDD awareness and reduce mortality, especially in older patients.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"9 ","pages":"Pages 54-58"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Senescence associated osteoarthritis: Emerging therapeutics and future directions","authors":"Sheen Razdan ,&nbsp;Anush Tomar ,&nbsp;Sweta Bawari","doi":"10.1016/j.clicom.2026.01.003","DOIUrl":"10.1016/j.clicom.2026.01.003","url":null,"abstract":"<div><div>Osteoarthritis is a degenerative condition that primarily affects the joints. This condition is often marked by the slow degradation of cartilage as well as changes in the subchondral bone. One of the key markers of osteoarthritis is chronic inflammation. Aging is a primary risk factor for osteoarthritis, as it leads to cellular senescence, which in turn causes degeneration of the bone and low-grade inflammation. Osteoarthritis is a major cause of disability, particularly affecting elderly people. With the increasing global population of elderly people, this condition is becoming a significant socioeconomic burden. Despite the increasing disease burden, there are no approved therapies to stop or reverse the progression of osteoarthritis. The current approved treatments only provide symptomatic care, which leads to the initiation of research in this field to develop novel therapies targeting its underlying mechanisms.</div><div>Emerging therapeutic strategies include senolytics and senomorphics, which aim to eliminate senescent cells or modulate their inflammatory secretory profiles. Senolytic agents such as Dasatinib can selectively induce apoptosis in senescent cells, showing efficacy in preclinical osteoarthritis models. Senomorphic agents, including Ruxolitinib, can mitigate inflammation by modulating cellular pathways like JAK-STAT, mTOR, AMPK, and Wnt/β-catenin signalling. Additionally, anti-inflammatory cytokine therapies targeting IL-17, IL-1, and IL-6 have demonstrated potential in preclinical and clinical studies by reducing osteoarthritis-associated inflammation and cartilage degradation.</div><div>This review focuses on the various cellular mechanisms through which bone tissues are degenerated due to cellular senescence, which highlights the key pathways or markers to be targeted to find novel therapeutics targeting cellular senescence. It also mentions some of the novel therapeutics of chemical, phytoconstituents, and biologics, which have shown positive results in various studies, but need further validation, and this can open a new horizon for research in this field.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"9 ","pages":"Pages 30-41"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146037929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neutrophils in obesity: from expansion to dysfunction","authors":"Nathalia Naranjo-Pinto ,&nbsp;Omar Rafael Alemán ,&nbsp;Carlos Rosales","doi":"10.1016/j.clicom.2026.05.005","DOIUrl":"10.1016/j.clicom.2026.05.005","url":null,"abstract":"<div><div>Obesity is associated with low-grade chronic inflammation and increased susceptibility to infections. A dysregulated immune response represents a central link between these processes. Neutrophils are key effector cells of the immune system that play essential roles in both inflammatory processes and host defense. Under physiological conditions, neutrophil numbers and functions are tightly regulated to maintain homeostasis. In obesity, however, this regulation becomes disrupted at multiple levels. Obesity promotes a sustained increase in circulating neutrophil numbers through enhanced granulopoiesis and increased release from the bone marrow. Despite this expansion, neutrophils do not exhibit improved antimicrobial capacity. Instead, they display a consistent pattern of functional dysregulation. At baseline, in obesity, neutrophils exhibit increased basal degranulation and extracellular reactive oxygen species production thus contributing to the inflammatory response. Likewise, neutrophil extracellular trap formation is favored in metabolically inflamed tissues, further contributing to inflammation. This apparent enhanced response of neutrophils is coupled with diminished responsiveness to infectious stimuli. While early events such as pathogen recognition and phagocytic uptake seem largely preserved, downstream mechanisms appear impaired. The result is a reduced intracellular microbial killing capacity and diminished neutrophil extracellular trap formation in response to pathogens. This functional dysregulation may be driven at least in part by changes in neutrophil metabolism. Current evidence indicates that metabolic reprogramming during obesity reshapes neutrophil function in a way that promotes inflammation while compromising host defense.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"9 ","pages":"Pages 151-164"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148177546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}