Pub Date : 2026-01-20DOI: 10.1016/j.clicom.2026.01.004
Arpita Mukherjee
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.
{"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":"2026-01-20","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}
There is paucity of data on recent trends of population-level deaths with Primary Immunodeficiency Diseases (PIDD).
Objective
To examine the population-based temporal trends in deaths with PIDD in the United States from 2015 to 2022.
Methods
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.
Results
The overall AAMR increased significantly from 2.5 to 3.5 (P < 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) [P = 0.03]. A similar trend was seen in several subgroups especially those aged ≥65 years.
Conclusion
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.
{"title":"Trends and contemporary epidemiology of mortality with primary immunodeficiency diseases in the United States, 2015–2022","authors":"Ernestina Bioh Hansen-Sackey , 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> < 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":"2026-01-17","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}
Pub Date : 2026-01-17DOI: 10.1016/j.clicom.2026.01.003
Sheen Razdan , Anush Tomar , Sweta Bawari
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.
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.
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.
{"title":"Senescence associated osteoarthritis: Emerging therapeutics and future directions","authors":"Sheen Razdan , Anush Tomar , 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":"2026-01-17","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}
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).
Methods
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.
Results
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 (P < 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 (P = 0.002).
Conclusion
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.
{"title":"Disease-specific clustering is seen among first-degree relatives in autoimmune rheumatic diseases: A cross-sectional, multi-centre study","authors":"S Chandrashekara , Padmanabha Shenoy , Uma Kumar , Sapan Pandya , Alakendu Ghosh , Rajkiran Dudam , Arghya Chattopadhyay , Apurva Khare , Rudra Prosad Goswami , 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> < 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":"2026-01-09","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}
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.
{"title":"Systems immunology meets clinical translation: Multi-omic approaches to predict therapy response in cancer and autoimmune disease","authors":"Praveen Kumar Chandra Sekar, 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":"2025-12-23","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}
Pub Date : 2025-12-11DOI: 10.1016/j.clicom.2025.12.001
Debora Rondinella , Ernesto Margarita , Pauline Celine Raoul , Francesca Sofia Galli , Andrea Severino , Serena Porcari , Maria Cristina Mele , Antonio Gasbarrini , Giovanni Cammarota , Emanuele Rinninella , Gianluca Ianiro
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.
{"title":"The impact of diet on gut microbiome composition: Implications for immune-mediated diseases","authors":"Debora Rondinella , Ernesto Margarita , Pauline Celine Raoul , Francesca Sofia Galli , Andrea Severino , Serena Porcari , Maria Cristina Mele , Antonio Gasbarrini , Giovanni Cammarota , Emanuele Rinninella , 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":"2025-12-11","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}
Pub Date : 2025-12-01DOI: 10.1016/j.clicom.2025.11.004
Betty Rachma , Rio Putra Pamungkas , Debi Yulia Sandra , Henry Sutanto , Deasy Fetarayani
Inflammatory bowel disease (IBD) and colorectal cancer (CRC) are intimately linked through complex immunological mechanisms that drive chronic inflammation and tumorigenesis. Persistent immune activation in IBD fosters a microenvironment conducive to malignant transformation, yet the precise molecular pathways underpinning this relationship remain an area of active investigation. Dysregulated interactions between innate and adaptive immune responses, aberrant cytokine signaling, and immune-modulating microbial factors contribute to the pathogenesis of both diseases. Advances in molecular immunology have revealed critical checkpoints and signaling cascades that may serve as therapeutic targets, offering new strategies for intervention. This review synthesizes current knowledge on the immunological landscape bridging these two conditions, emphasizing translational implications and future research directions. By delineating key molecular pathways and immune dynamics, this work aims to provide a comprehensive perspective on the interplay between chronic inflammation and colorectal tumorigenesis, fostering a deeper understanding of potential diagnostic and therapeutic advancements.
{"title":"The immunological nexus between inflammatory bowel disease and colorectal cancer: A molecular perspective","authors":"Betty Rachma , Rio Putra Pamungkas , Debi Yulia Sandra , Henry Sutanto , Deasy Fetarayani","doi":"10.1016/j.clicom.2025.11.004","DOIUrl":"10.1016/j.clicom.2025.11.004","url":null,"abstract":"<div><div>Inflammatory bowel disease (IBD) and colorectal cancer (CRC) are intimately linked through complex immunological mechanisms that drive chronic inflammation and tumorigenesis. Persistent immune activation in IBD fosters a microenvironment conducive to malignant transformation, yet the precise molecular pathways underpinning this relationship remain an area of active investigation. Dysregulated interactions between innate and adaptive immune responses, aberrant cytokine signaling, and immune-modulating microbial factors contribute to the pathogenesis of both diseases. Advances in molecular immunology have revealed critical checkpoints and signaling cascades that may serve as therapeutic targets, offering new strategies for intervention. This review synthesizes current knowledge on the immunological landscape bridging these two conditions, emphasizing translational implications and future research directions. By delineating key molecular pathways and immune dynamics, this work aims to provide a comprehensive perspective on the interplay between chronic inflammation and colorectal tumorigenesis, fostering a deeper understanding of potential diagnostic and therapeutic advancements.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"8 ","pages":"Pages 138-158"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683792","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}
Pub Date : 2025-11-11DOI: 10.1016/j.clicom.2025.11.003
Sithi Sarkar, Sailee Chowdhury, Koyel Kar, Priyanka Chakraborty, Anirban Das
The rise of multiantibiotic-resistant bacteria poses a major challenge to infection management, as some bacteria survive even antibiotic therapy by evading immune responses. With decreasing treatment options due to increased antibiotic resistance, there is an urgent need for alternative or adjunctive therapies. Immunotherapy, widely used in cancer treatment for its ability to overcome immunosuppression, is emerging as a promising approach for bacterial infections, including persistent and drug-resistant diseases like tuberculosis. Strategies such as immune checkpoint inhibition, cytokine modulation, and cellular therapies are demonstrating potential in preclinical studies. These approaches aim to restore or enhance host immunity against bacterial pathogens. Given the growing threat of resistance, advancing immunotherapy into clinical use requires rigorous trials to validate safety and efficacy. This review discusses the therapeutic promise of immunotherapies against bacterial infections, highlights recent advancements, and outlines current and future directions in the field.
{"title":"Immunological interventions in bacterial infections: From mechanisms to clinical applications","authors":"Sithi Sarkar, Sailee Chowdhury, Koyel Kar, Priyanka Chakraborty, Anirban Das","doi":"10.1016/j.clicom.2025.11.003","DOIUrl":"10.1016/j.clicom.2025.11.003","url":null,"abstract":"<div><div>The rise of multiantibiotic-resistant bacteria poses a major challenge to infection management, as some bacteria survive even antibiotic therapy by evading immune responses. With decreasing treatment options due to increased antibiotic resistance, there is an urgent need for alternative or adjunctive therapies. Immunotherapy, widely used in cancer treatment for its ability to overcome immunosuppression, is emerging as a promising approach for bacterial infections, including persistent and drug-resistant diseases like tuberculosis. Strategies such as immune checkpoint inhibition, cytokine modulation, and cellular therapies are demonstrating potential in preclinical studies. These approaches aim to restore or enhance host immunity against bacterial pathogens. Given the growing threat of resistance, advancing immunotherapy into clinical use requires rigorous trials to validate safety and efficacy. This review discusses the therapeutic promise of immunotherapies against bacterial infections, highlights recent advancements, and outlines current and future directions in the field.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"8 ","pages":"Pages 124-137"},"PeriodicalIF":0.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145570911","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}
Pub Date : 2025-11-11DOI: 10.1016/j.clicom.2025.11.002
Abduarahman Almutairi , Amal Alzaby , Mohammed Albayedh , Abdulrahman N. AlJaber , Muteb Altowairqi
ACT1 deficiency is extremely rare inborn error of immunity with only eleven cases reported in the literature. We reported a case series of three Saudi patients with chronic mucocutaneous candidiasis (CMC) due to mutations in TRAF3IP2, a gene encoding the adaptor ACT1. Two of them were siblings who presented with recurrent oral thrush, hair folliculitis, and short stature, and were found to have a frameshift TRAF3IP2 mutation. The other patient had recurrent oral thrush complicated with candida esophagitis. He also demonstrated characteristics indicative of attention-deficit/hyperactivity disorder (ADHD). He harbored a nonsense TRAF3IP2 mutation. Short stature and ADHD are clinical manifestations not previously linked to ACT1 deficiency, suggesting the potential for more broader systemic involvement. In this manuscript, we delineate additional cases that expand the clinical and genetic landscape of TRAF3IP2-associated disorders.
{"title":"Chronic mucocutaneous candidiasis due to TRAF3IP2 mutation in three Saudi patients – A case series and literature review","authors":"Abduarahman Almutairi , Amal Alzaby , Mohammed Albayedh , Abdulrahman N. AlJaber , Muteb Altowairqi","doi":"10.1016/j.clicom.2025.11.002","DOIUrl":"10.1016/j.clicom.2025.11.002","url":null,"abstract":"<div><div>ACT1 deficiency is extremely rare inborn error of immunity with only eleven cases reported in the literature. We reported a case series of three Saudi patients with chronic mucocutaneous candidiasis (CMC) due to mutations in TRAF3IP2, a gene encoding the adaptor ACT1. Two of them were siblings who presented with recurrent oral thrush, hair folliculitis, and short stature, and were found to have a frameshift TRAF3IP2 mutation. The other patient had recurrent oral thrush complicated with candida esophagitis. He also demonstrated characteristics indicative of attention-deficit/hyperactivity disorder (ADHD). He harbored a nonsense TRAF3IP2 mutation. Short stature and ADHD are clinical manifestations not previously linked to ACT1 deficiency, suggesting the potential for more broader systemic involvement. In this manuscript, we delineate additional cases that expand the clinical and genetic landscape of TRAF3IP2-associated disorders.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"8 ","pages":"Pages 120-123"},"PeriodicalIF":0.0,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145519437","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}
Pub Date : 2025-11-07DOI: 10.1016/j.clicom.2025.11.001
Jainu Ajit , Rebeka Ambrožič
Cancer patients experience a significant symptom burden that affects their quality of life. These include gastrointestinal, neurological, and physical side effects, which worsen fatigue and quality of life during conventional treatments like radiotherapy, chemotherapy, and immunotherapy. Consequently, there is increasing interest in integrative approaches to complement standard treatments. Among these, medicinal mushrooms are gaining popularity because of their immunomodulatory properties and potential to alleviate common cancer- and treatment-related symptoms. We thoroughly review existing reports on the benefits of medicinal mushrooms in cancer care and discuss how future clinical trials can apply more rigorous methods to quantitatively assess their advantages.
{"title":"Medicinal mushroom-derived compounds for managing neuro-gastrointestinal and physical symptoms in cancer patients: Mechanisms, clinical evidence, and future directions","authors":"Jainu Ajit , Rebeka Ambrožič","doi":"10.1016/j.clicom.2025.11.001","DOIUrl":"10.1016/j.clicom.2025.11.001","url":null,"abstract":"<div><div>Cancer patients experience a significant symptom burden that affects their quality of life. These include gastrointestinal, neurological, and physical side effects, which worsen fatigue and quality of life during conventional treatments like radiotherapy, chemotherapy, and immunotherapy. Consequently, there is increasing interest in integrative approaches to complement standard treatments. Among these, medicinal mushrooms are gaining popularity because of their immunomodulatory properties and potential to alleviate common cancer- and treatment-related symptoms. We thoroughly review existing reports on the benefits of medicinal mushrooms in cancer care and discuss how future clinical trials can apply more rigorous methods to quantitatively assess their advantages.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"8 ","pages":"Pages 109-119"},"PeriodicalIF":0.0,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145519438","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}
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