Clinical Immunology Communications最新文献

{"title":"The immunological nexus between inflammatory bowel disease and colorectal cancer: A molecular perspective","authors":"Betty Rachma ,&nbsp;Rio Putra Pamungkas ,&nbsp;Debi Yulia Sandra ,&nbsp;Henry Sutanto ,&nbsp;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}

{"title":"Papillon-Lefèvre syndrome presenting with early-onset Psoriasis and Osteomyelitis: A case report","authors":"Aisha Mirza ,&nbsp;Batoul Basalom ,&nbsp;Mohammed H Almatrafi ,&nbsp;Ameera Bukhari ,&nbsp;Amer Khojah","doi":"10.1016/j.clicom.2025.10.002","DOIUrl":"10.1016/j.clicom.2025.10.002","url":null,"abstract":"<div><div>Papillon-Lefèvre syndrome (PLS) is a rare autosomal recessive disorder caused by mutations in the Cathepsin C (CTSC) gene, characterized by palmoplantar hyperkeratosis, severe periodontitis, and recurrent infections. We present the case of an 8-year-old boy with early-onset psoriasis diagnosed in infancy and managed with Adalimumab. He presented with progressive right knee swelling, and intermittent fever. MRI revealed a Brodie abscess with features of osteomyelitis. Abscess fluid culture was positive for methicillin-resistant <em>Staphylococcus aureus</em>. Whole-exome sequencing identified a homozygous missense variant in the CTSC gene (c.899G&gt;<em>A</em>; p.Gly300Asp), confirming the diagnosis of PLS. Interestingly, his dental panoramic x-ray was normal. This case underscores the importance of genetic testing in patients with early-onset psoriasis and atypical infections. Although almost all reported cases of PLS feature early, severe periodontitis, our patient did not show dental involvement. This highlights that younger patients with PLS may present without this classical feature.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"8 ","pages":"Pages 101-104"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145465706","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":"Assessment of CD38brightHLA-DR+ T cells using a rapid flow cytometry-based assay to aid in the diagnosis of hemophagocytic lymphohistiocytosis and immune regulatory disorders in adult subjects","authors":"Aaruni Khanolkar,&nbsp;Erin Weyers,&nbsp;Ramakrishna Sompallae,&nbsp;Matthew D. Krasowski","doi":"10.1016/j.clicom.2025.05.004","DOIUrl":"10.1016/j.clicom.2025.05.004","url":null,"abstract":"<div><div>Rapid and accurate diagnosis of patients suspected of suffering from hyperinflammatory conditions such as hemophagocytic lymphohistiocytosis (HLH) is a critical aspect of timely management for such disorders. Soluble IL-2Rα (sIL-2Rα) and plasma ferritin constitute the mainstay of frontline laboratory investigations performed to establish a clinical diagnosis for these patients. However, there is a paucity of clinical laboratories that perform the sIL-2Rα measurement as a <em>stat</em> test which can delay the diagnosis and management of these patients. Consequently, rapid flow cytometry-based tests that measure T cell activation are currently being evaluated. Previous studies have examined the utility of flow-cytometry based testing in pediatric subjects with HLH and immune dysregulation disorders. In this report, we assessed the utility of our flow-cytometry based test in adult patients suspected of HLH and discuss its performance in relation to what has been reported previously in the literature for pediatric patients.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"8 ","pages":"Pages 1-5"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144230518","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":"Reprogramming immunity: Emerging therapeutic frontiers and clinical trial advances of CAR-T cell therapy in autoimmune diseases","authors":"Arpita Mukherjee","doi":"10.1016/j.clicom.2025.09.003","DOIUrl":"10.1016/j.clicom.2025.09.003","url":null,"abstract":"<div><div>Autoimmune diseases result from a breakdown in immune tolerance, leading to chronic activation of autoreactive lymphocytes. Conventional therapies offer symptomatic relief but rarely achieve durable remission. Chimeric antigen receptor (CAR)-T cell therapy, originally developed for hematologic malignancies, is now being repurposed to selectively deplete pathogenic immune subsets in autoimmunity. This review explores how CAR-T cells may not only eliminate autoreactive B and T cells but also reprogram immune homeostasis toward long-term tolerance. Recent clinical success with CD19-directed CAR-T cells in refractory systemic lupus erythematosus underscores this paradigm shift. Furthermore, next-generation constructs including dual CARs, inhibitory CARs (iCARs), and CAR-Tregs offer innovative strategies to balance cytotoxicity with regulatory control. Key challenges such as antigen escape, off-target effects, and therapeutic accessibility are critically analyzed within current translational and clinical landscapes. This work advocates for a mechanistically guided redefinition of autoimmune therapy through precision-engineered immune reprogramming.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"8 ","pages":"Pages 60-74"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145095119","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":"CASPASE-3 expression and activity in PBMCs associate with SARS-CoV-2 infection and clinical features","authors":"Vanessa Mylenna Florêncio de Carvalho ,&nbsp;Bárbara de Oliveira Silva ,&nbsp;Priscilla Stela Santana de Oliveira ,&nbsp;Thacianna Barreto da Costa ,&nbsp;Michelle Melgarejo da Rosa ,&nbsp;Moacyr Jesus Barreto de Melo Rêgo ,&nbsp;Michelly Cristiny Pereira ,&nbsp;Maira Galdino da Rocha Pitta","doi":"10.1016/j.clicom.2025.09.004","DOIUrl":"10.1016/j.clicom.2025.09.004","url":null,"abstract":"<div><h3>Background</h3><div>Although vaccines and treatments exist, new SARS-CoV-2 variants continue to emerge. An imbalance between apoptosis and autophagy may contribute to COVID-19 pathogenesis, leading to tissue damage and inflammation.</div></div><div><h3>Objective</h3><div>To investigate the role of cell death-related proteins during SARS-CoV-2 infection and their associations with clinical variables.</div></div><div><h3>Methods</h3><div>A total of 140 samples were analyzed (<em>n</em> = 73 infected, <em>n</em> = 67 uninfected). Gene expression of apoptotic and autophagic markers was evaluated by RT-qPCR in peripheral blood mononuclear cells. Caspase 3/7 activity was assessed using flow cytometry.</div></div><div><h3>Results</h3><div>Infected patients showed higher expression of CASPASE 3, BID (<em>p</em> &lt; 0.05), and MAP1LC3 (<em>p</em> &lt; 0.01). CASPASE 3 expression was higher in variant omicron, male sex, high viral load, and various clinical symptoms. Caspase 3/7 activity increased in CD4⁺ T and B cells of individuals infected with SARS-CoV-2.</div></div><div><h3>Conclusions</h3><div>Although our previous results with CASPASE 3 are promising and suggest that it may become a potential therapeutic target, additional studies are needed to confirm these hypotheses and evaluate potential intervention strategies.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"8 ","pages":"Pages 81-89"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145218944","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":"Profiling the serum cytokine B cell activating factor (BAFF),proliferation inducing ligand (APRIL), and BP180, BP230 antibodies in bullous pemphigoid patients before and after treatment: a prospective case-control study","authors":"Shadab Seraji ,&nbsp;Kamran Balighi ,&nbsp;Amir Hooshang Ehsani ,&nbsp;Ala Ehsani ,&nbsp;Hamidreza Mahmoudi ,&nbsp;Maryam Daneshpazhooh ,&nbsp;Pedram Noormohammadpour ,&nbsp;Saman Al Zahawi ,&nbsp;Zeinab Aryanian ,&nbsp;Parvaneh Hatami","doi":"10.1016/j.clicom.2025.09.002","DOIUrl":"10.1016/j.clicom.2025.09.002","url":null,"abstract":"<div><h3>Background</h3><div>Bullous pemphigoid is a subepidermal autoimmune blistering disease caused by auto-antibodies directed against specific components of the basement membrane molecules. It has been shown that T cell function and B cell survival depend on B-cell activating factor (BAFF), a member of the tumor necrosis factor superfamily. Its contribution to the formation of BP is yet unknown, though.</div></div><div><h3>Aim</h3><div>To measure the serum level of cytokines B cell activating factor (BAFF) and proliferation inducing ligand (APRIL), as well as BP180 and BP230 antibodies in patients with bullous pemphigoid before and after treatment.</div></div><div><h3>Methods</h3><div>New patients with a confirmed diagnosis of bullous pemphigoid from a tertiary care hospital were selected. After obtaining written consent, blood samples were taken according to the required standards, and the levels of the above indices were checked before and four months after treatment.</div></div><div><h3>Results</h3><div>This prospective case-control study recruited 32 patients with newly diagnosed BP and 24 healthy controls. Based on the obtained results, BAFF and APRIL levels were higher in the case group than the control group both before and after the treatment. Specifically, the changes in the BAFF index were statistically significant in both conditions: before treatment compared to controls (<em>P</em> = 0.001) and after treatment compared to controls (<em>P</em> = 0.015). Similarly, significant changes were observed in the APRIL index for the cases when comparing before treatment to controls (<em>P</em> &lt; 0.001). Interestingly, those who have been treated with rituximab experienced a high level of BAFF even after treatment and in comparison with the healthy group but a decline in APRIL, BP180, and BP230.</div></div><div><h3>Conclusions</h3><div>The results of this study showed a decrease in APRIL, BP180, and BP230 indices in patients with Bullous pemphigoid after treatment in accordance with clinical improvement and remission. This study is one step forward in elaborating the role of BAFF and APRIL in the pathogenesis and monitoring of patients with BP.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"8 ","pages":"Pages 75-80"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145095120","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":"Paraneoplastic neurologic syndromes in breast cancer: Immunological mechanisms and therapeutic insights","authors":"Carolina Coradi ,&nbsp;Beatriz Geovana Leite Vacario ,&nbsp;Marina Rayciki Sotomayor ,&nbsp;Victor Pereira da Silva ,&nbsp;Gabriela Bonetti Bellandi ,&nbsp;Luísa Cristina Fortuna da Silva ,&nbsp;Carlos Frederico de Almeida ,&nbsp;Carolina Panis","doi":"10.1016/j.clicom.2025.06.003","DOIUrl":"10.1016/j.clicom.2025.06.003","url":null,"abstract":"<div><div>Research into paraneoplastic neurologic syndromes (PNS) has advanced significantly. This progress is reflected in the continuous refinement of diagnostic criteria and the introduction of novel antibodies for research purposes. Recently, there have been insights into the involvement of T cells in the pathophysiology of certain PNS, although many aspects of the underlying mechanisms remain to be fully understood. In breast cancer, there is emerging evidence linking drug treatments to the onset of PNS, and associated molecular mechanisms enrolling the immune system have been delineated. Here, we explore the evolving understanding of paraneoplastic neurologic syndrome development in breast cancer patients, emphasizing the immunological molecular pathways involved and the role of cytotoxic chemotherapy and immunotherapy in this context.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"8 ","pages":"Pages 26-37"},"PeriodicalIF":0.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144564050","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":"Expansion of SARS-CoV-2 mutations in patient with B-cell lymphoma and rare combination of ACE2, TLR4, DDX58 and IFIH1 variations: A retrospective analysis of the virus-host interplay","authors":"Angelina Trifonova ,&nbsp;Adelina Yosifova ,&nbsp;Atanas Syarov ,&nbsp;Andrey Velichkov ,&nbsp;Martin Pasev ,&nbsp;Svetlomir Takov ,&nbsp;Kalina Madarzhieva ,&nbsp;Krassimir Angelov ,&nbsp;Radoslava Vazharova ,&nbsp;Velislava Terzieva","doi":"10.1016/j.clicom.2025.02.001","DOIUrl":"10.1016/j.clicom.2025.02.001","url":null,"abstract":"<div><div>Lessons from the COVID-19 outbreak suggest a highly variable individual clinical course of infection and unpredictable outcomes among infected individuals. In this retrospective study, we examined the intra-host viral evolution in an immunocompromised patient with B-cell lymphoma, severe COVID-19, and a two-stage, long-lasting in-hospital period with lethal outcome. The whole-genome sequencing profile demonstrated a dynamic accumulation of new viral mutations in the entire viral genome, mainly in S1-RBD and Nsp12, against the background of antiviral treatment and convalescent plasma transfusion. Long range-PCR and nanopore sequencing of <em>ACE2, TLR7, TLR8, TLR4, DDX58,</em> and <em>IFIH1</em> genes revealed single nucleotide substitutions in the ACE2, TLR4, DDX58, IFIH1, and TLR7 receptors, negatively affecting the disease course from the onset. Our results demonstrate that genetic variations in host innate immunity and impaired adaptive immunity facilitate the accumulation of viral mutations that overcome antiviral treatment and passive antibody transfer, affecting the course of SARS-CoV-2 infection.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"7 ","pages":"Pages 47-54"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143577284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gal-9: A potential game-changer in COVID-19 severity assessment","authors":"Eduardo Davi Lima da Silva ,&nbsp;Heloisa Isabela Leão ,&nbsp;Ryan Cordeiro Silva ,&nbsp;Nathália Tavares Ferreira ,&nbsp;Amanda Pinheiro de Barros Albuquerque ,&nbsp;André Machado de Siqueira ,&nbsp;Michelly Cristiny Pereira ,&nbsp;Michelle Melgarejo da Rosa ,&nbsp;Moacyr Jesus Barreto de Melo Rêgo ,&nbsp;Maira Galdino da Rocha Pitta","doi":"10.1016/j.clicom.2025.05.002","DOIUrl":"10.1016/j.clicom.2025.05.002","url":null,"abstract":"<div><h3>Background</h3><div>This study investigates Galectin-9 (Gal-9) as a potential biomarker for COVID-19 severity, aiming to improve patient stratification and guide clinical management.</div></div><div><h3>Design and methods</h3><div>We analyzed Gal-9 levels (blood and saliva) in 112 mild, 57 severe COVID-19 patients, 93 symptomatic non-COVID-19 individuals, and 70 controls (healthy controls) using ELISA and RT-qPCR.</div></div><div><h3>Results</h3><div>Both mild and severe COVID-19 patients exhibited elevated Galectin-9 (Gal-9) levels, with severe cases showing significantly higher serum levels (mRNA and protein) compared to mild or healthy controls. This suggests Galectin-9 involvement in the acute phase, as levels declined within 15 days post-diagnosis. Fever and cough correlated with disease severity. ROC analysis demonstrated high accuracy in patient stratification. Furthermore, we detected elevated Galectin-9 protein in the saliva of individuals with mild COVID-19, highlighting its potential as a non-invasive biomarker for early disease detection.</div></div><div><h3>Conclusion</h3><div>This study identifies Gal-9 as a promising biomarker for COVID-19 severity. Elevated Gal-9 levels hold potential for improved patient stratification and clinical management, highlighting the importance of biomarker research in understanding COVID-19 pathophysiology.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"7 ","pages":"Pages 64-71"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144068560","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":"Serological responses to SARS-CoV-2 in vaccinated and unvaccinated individuals: A Canadian study","authors":"Andrea Monjo ,&nbsp;Tania Rodríguez-Ramos ,&nbsp;Mark R. Bruder ,&nbsp;Nguyen T.K. Vo ,&nbsp;Mark Oremus ,&nbsp;Kevin J. Stinson ,&nbsp;Brian Dixon ,&nbsp;Marc G Aucoin","doi":"10.1016/j.clicom.2025.02.002","DOIUrl":"10.1016/j.clicom.2025.02.002","url":null,"abstract":"<div><div>COVID-19 severity has been correlated with older age, male sex, and the presence of comorbidities; it is hypothesized that SARS-CoV-2 antibody responses are also correlated.159 unvaccinated patients with SARS-CoV-2 infections were assessed for IgA, IgG, and IgM titers, which were compared with disease severity, age, sex, presence of comorbidities, and time since infection. Anti-S and anti-Nucleocapsid (N) IgG responses were compared between unvaccinated and vaccinated SARS-CoV-2 positive patients. Anti-S IgA and IgM were better indicators of disease severity than IgG. IgG responses were more likely for patients over 60 years old. Female patients over 60 were more likely to have an antibody response than female patients under 60. Vaccinated patients had a stronger IgG response against S protein than against N protein likely due to immune imprinting. Disease severity was correlated with anti-S antibody responses and comorbidities in unvaccinated patients.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"7 ","pages":"Pages 39-46"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143549428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}