Andrea Monjo , Tania Rodríguez-Ramos , Mark R. Bruder , Nguyen T.K. Vo , Mark Oremus , Kevin J. Stinson , Brian Dixon , Marc G Aucoin
{"title":"Serological responses to SARS-CoV-2 in vaccinated and unvaccinated individuals: A Canadian study","authors":"Andrea Monjo , Tania Rodríguez-Ramos , Mark R. Bruder , Nguyen T.K. Vo , Mark Oremus , Kevin J. Stinson , Brian Dixon , 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":"2025-02-28","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}
{"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 , Adelina Yosifova , Atanas Syarov , Andrey Velichkov , Martin Pasev , Svetlomir Takov , Kalina Madarzhieva , Krassimir Angelov , Radoslava Vazharova , 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":"2025-02-28","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}
Muhammad Adnan Zaman , Tahlyn Miller , Warsha Korani , Mina Jilani
{"title":"Fever of unknown origin in a dialysis patient: A case report of dialyzer membrane allergy","authors":"Muhammad Adnan Zaman , Tahlyn Miller , Warsha Korani , Mina Jilani","doi":"10.1016/j.clicom.2025.01.001","DOIUrl":"10.1016/j.clicom.2025.01.001","url":null,"abstract":"<div><div>Fever following hemodialysis presents a diagnostic challenge, often raising concerns about infection. However, non-infectious causes, such as allergic reactions to dialysis membranes, must also be considered. Dialyzer-related reactions, particularly to synthetic membranes like polysulfone, are increasingly recognized as contributors to post-dialysis fever. Although modern dialysis technology has improved biocompatibility by eliminating acetate buffers and sterilizing ethylene oxide, acute hypersensitivity reactions still occur. These reactions are classified into Type A (anaphylactic) and Type B (non-anaphylactic), each with distinct symptoms. Proper identification of these reactions is essential for management, as switching to a more biocompatible membrane is often required. This case report describes a 38-year-old male who developed a fever after hemodialysis in a prison facility. Initial workup ruled out infection, with negative blood cultures and elevated IgE levels suggesting a hypersensitivity reaction to the polysulfone membrane. The patient's symptoms resolved following a switch to a hypoallergenic dialyzer.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"7 ","pages":"Pages 34-38"},"PeriodicalIF":0.0,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143167299","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}
Venkata Yeramilli , Michael Harper , Riadh Cheddadi , Colin Martin
{"title":"Maternal prenatal stress modulates antibody levels in offspring","authors":"Venkata Yeramilli , Michael Harper , Riadh Cheddadi , Colin Martin","doi":"10.1016/j.clicom.2024.12.003","DOIUrl":"10.1016/j.clicom.2024.12.003","url":null,"abstract":"<div><div>Maternal stress is a risk factor for preterm birth and is associated with adverse birth outcomes and immune adaptations in the baby. In this study, we used a murine model of prenatal stress and measured serum immunoglobulin levels in the dams and offspring following stress. We found a significant decrease in the levels of all IgG subclasses in dams following stress. In contrast, we observed an increase in the levels of IgG1, IgG2b and IgG3 in the offspring derived from stressed dams compared to unstressed controls. We made similar observations in offspring that were fed corticosterone in drinking water during gestation indicating that these changes in immunoglobulin (Ig) levels are mediated by excess cortisol. Overall, the results from these studies will help better understand the casual link between prenatal maternal stress and compromised neonatal immunity and will help develop optimal vaccination strategies to protect both the pregnant women and infant.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"7 ","pages":"Pages 27-33"},"PeriodicalIF":0.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143167298","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":"Involvement of β-glucan receptors on the antitumor activity of β-glucans","authors":"Atsushi Iwai","doi":"10.1016/j.clicom.2024.12.002","DOIUrl":"10.1016/j.clicom.2024.12.002","url":null,"abstract":"<div><div>β-glucans consisting of β-(1,3)-linked glucose as the main chain (hereafter simply called “β-glucan”) are suggested to have the potential for many beneficial effects on health. Among known beneficial effects, the most notable effect of β-glucan would be the antitumor effect. The antitumor effect of β-glucan has been known since the mid-twentieth century. In current cancer treatments where immune checkpoint inhibitors are attracting attention, it is expected that the combined administration of β-glucan will exhibit a greater therapeutic effect. The antitumor effect of β-glucan is believed to be closely linked to the receptors that recognize β-glucan. On the other hand, it has been clarified that there are many receptors for the recognition of β-glucan, in addition to CR3 (complement receptor 3) and dectin-1 (dendritic cell-associated C-type lectin-1), the well-known β-glucan receptors. This review focused on various β-glucan receptors reported previously and discusses the molecular mechanisms through which β-glucans exhibit antitumor effects.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"7 ","pages":"Pages 1-17"},"PeriodicalIF":0.0,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143167300","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":"Role of skin antimicrobial peptides in the pathogenesis of psoriasis, atopic dermatitis and hidradenitis suppurative: Highlights on dermcidin","authors":"José E Belizário","doi":"10.1016/j.clicom.2024.12.001","DOIUrl":"10.1016/j.clicom.2024.12.001","url":null,"abstract":"<div><div>Diverse classes of antimicrobial peptides (AMPs) produced by keratinocytes, sebocytes, epithelial cells of apocrine and eccrine sweat glands and innate immune cells are continually released in the skin tissue layers. Together they exert the fine homeostatic control of the host immune cells-skin microbiome interactions, inhibiting bacterial overgrowth and skin barrier disruption. Under a variety of pathological conditions, up or down regulation of AMP expression can contribute to microbial diversity imbalance or dysbiosis, which can initiate or worsen the most common cutaneous diseases. This review updates on the roles of dermcidin, defensins, cathelicidins and S100 proteins as modulators of microbiomes, inflammation and recurrent bacterial infections in psoriasis, atopic dermatitis and hidradenitis suppurativa. The top most significant disease-immune signaling pathways mediated by the cytokines IL-1, TNF-α, IL-17, IL-23 and IL-33 are also reviewed. Current studies suggest that raising and lowering of host cell- and bacterial-derived AMPs may directly affect microbiome and immunity homeostasis at local body sites. Molecular genetics and microbiome studies should help us to investigate the bacterial species and AMPs synergistic or harmful interactions with causal gene variants, harnessing their potential clinical application in the journey of skin disease patients.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"7 ","pages":"Pages 18-26"},"PeriodicalIF":0.0,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143167297","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":"Long-term follow-up of anti-IFN-α2 autoantibody levels in hospitalized individuals with COVID-19","authors":"Maaike Cockx , Nick Geukens , Birthe Michiels , Doreen Dillaerts , Eveline Claeys , Olivia Vandekerckhove , Natalie Lorent , Xavier Bossuyt","doi":"10.1016/j.clicom.2024.11.001","DOIUrl":"10.1016/j.clicom.2024.11.001","url":null,"abstract":"<div><div>Anti-type-I interferon (IFN) autoantibodies have been associated with severe COVID-19. Their association with long COVID, however, is unclear.</div><div>Anti-IFN-α2 antibody levels were followed-up for one year in individuals hospitalized for acute COVID-19 (n=97). Specific anti-IFN-α2 antibodies were detected in 5/97 patients. High anti-IFN-α2 antibody levels during acute infection were only detected in patients admitted to ICU (3/42), of whom 2 had persistent high levels and residual changes on chest computed tomography 12 months post-infection. Two patients not admitted to ICU had undetectable antibodies during acute infection, but had low detectable antibody levels 12 months post-infection; one of whom suffered from long COVID.</div><div>In conclusion, anti-IFN-α2 antibodies during acute infection are not associated with post-SARS-CoV-2 residual sequelae. Two patients with initially undetectable anti-IFN-α2 autoantibodies showed increased autoantibody levels 12 months post-infection. Additional large studies are needed to study the potential role of loss of tolerance after SARS-CoV-2 infection in long COVID.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"6 ","pages":"Pages 26-30"},"PeriodicalIF":0.0,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142700055","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":"CRISPR/Cas9-mediated RELA and RELC knockout in human regulatory T cells abrogates FOXP3 expression and suppressive function","authors":"Yohei Sato , Yamato Hanawa , Akihito Tsubota","doi":"10.1016/j.clicom.2024.10.002","DOIUrl":"10.1016/j.clicom.2024.10.002","url":null,"abstract":"<div><div>Mutations in NF-κB-related molecules result in combined immunodeficiency characterized by recurrent infection. In this study, we aimed to investigate the association between mutations in NF-κB family members, RELA, RELB, and RELC, and regulatory T cell (Treg) function in humans. <em>RELA, RELB</em>, and <em>RELC</em> were knocked out using CRISPR/Cas9-mediated homologous recombination in CD4<sup>+</sup>/CD8<sup>+</sup> T cells and Tregs isolated from healthy donors. The <em>RELA, RELB</em>, and <em>RELC</em> knockouts did not alter the phenotype or cytokine production profile of CD4<sup>+</sup>/CD8<sup>+</sup> T cells or Jurkat cells. Similar to that observed in knockout mice, <em>RELA</em> or <em>RELC</em> knockout in MT-2 cells and freshly isolated Tregs reduced FOXP3 expression and the immune suppressive function of Tregs. Additionally, PD-L1 expression in effector T cells and Tregs decreased considerably following RELC knockdown. These findings demonstrated that the deletion of RELA or RELC resulted in the loss of Treg-like phenotype and function owing to the downregulation of FOXP3 expression.</div></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"6 ","pages":"Pages 15-25"},"PeriodicalIF":0.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142536085","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":"Deficiency of interleukin-1 receptor antagonist: An updated review of the pathogenesis, clinical characteristics, and treatments","authors":"Spencer Fang , Joshua Pillai , Baharullah Mahin","doi":"10.1016/j.clicom.2024.09.001","DOIUrl":"10.1016/j.clicom.2024.09.001","url":null,"abstract":"<div><p>Deficiency of Interleukin-1 receptor antagonist (DIRA) is a rare autosomal recessive autoinflammatory disease first reported in 2009. To date, 33 patients have been previously characterized and reported in literature. To the best of our knowledge, there have been no recent studies that have broadly evaluated recent advances in understanding of this challenging and life-threatening condition. Herein, we comprehensively reviewed the etiology and cytogenetic abnormalities of DIRA. We then investigated the current diagnostics used for identifying the variants of this disease. Furthermore, we report the demographics and characteristics broadly found in the current patient sample. Lastly, we discuss the treatments (antibiotics, corticosteroids, etc.) and the primary biologics (anakinra, canakinumab, adalimumab, and rilonacept) used in patients, along with current information on their clinical safety and efficacy. Overall, although further investigations are required for this disease, this review may be informative to clinicians treating and managing patients presenting with DIRA.</p></div>","PeriodicalId":100269,"journal":{"name":"Clinical Immunology Communications","volume":"6 ","pages":"Pages 9-14"},"PeriodicalIF":0.0,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772613424000131/pdfft?md5=efd31efbf265a26f98baec737ce483c3&pid=1-s2.0-S2772613424000131-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142168609","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}