Clinical Immunology Communications最新文献

Fever of unknown origin in a dialysis patient: A case report of dialyzer membrane allergy

Clinical Immunology Communications Pub Date : 2025-01-09 DOI: 10.1016/j.clicom.2025.01.001

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}

引用次数: 0

Maternal prenatal stress modulates antibody levels in offspring

Clinical Immunology Communications Pub Date : 2024-12-18 DOI: 10.1016/j.clicom.2024.12.003

Venkata Yeramilli , Michael Harper , Riadh Cheddadi , Colin Martin

引用次数: 0

Involvement of β-glucan receptors on the antitumor activity of β-glucans

Clinical Immunology Communications Pub Date : 2024-12-15 DOI: 10.1016/j.clicom.2024.12.002

Atsushi Iwai

引用次数: 0

Role of skin antimicrobial peptides in the pathogenesis of psoriasis, atopic dermatitis and hidradenitis suppurative: Highlights on dermcidin

Clinical Immunology Communications Pub Date : 2024-12-13 DOI: 10.1016/j.clicom.2024.12.001

José E Belizário

{"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}

引用次数: 0

Corrigendum to “Beneficial immune-regulatory effects of novel strains of Aureobasidium pullulansAFO-202 and N-163 produced beta glucans in Sprague Dawley rats” [Clinical Immunology Communications 1 (2021) 29–34]

Clinical Immunology Communications Pub Date : 2024-12-01 DOI: 10.1016/j.clicom.2024.10.001

Nobunao Ikewaki , Kadalraja Raghavan , Vidyasagar Devaprasad Dedeepiya , Suryaprakash Vaddi , Masaru Iwasaki , Rajappa Senthilkumar , Senthilkumar Preethy , Samuel JK Abraham

引用次数: 0

Long-term follow-up of anti-IFN-α2 autoantibody levels in hospitalized individuals with COVID-19 对 COVID-19 住院患者的抗-IFN-α2 自身抗体水平进行长期随访

Clinical Immunology Communications Pub Date : 2024-11-17 DOI: 10.1016/j.clicom.2024.11.001

Maaike Cockx , Nick Geukens , Birthe Michiels , Doreen Dillaerts , Eveline Claeys , Olivia Vandekerckhove , Natalie Lorent , Xavier Bossuyt

{"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}

引用次数: 0

CRISPR/Cas9-mediated RELA and RELC knockout in human regulatory T cells abrogates FOXP3 expression and suppressive function CRISPR/Cas9 介导的人调节性 T 细胞中 RELA 和 RELC 基因敲除可抑制 FOXP3 的表达和抑制功能

Clinical Immunology Communications Pub Date : 2024-10-18 DOI: 10.1016/j.clicom.2024.10.002

Yohei Sato , Yamato Hanawa , Akihito Tsubota

{"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}

引用次数: 0

Deficiency of interleukin-1 receptor antagonist: An updated review of the pathogenesis, clinical characteristics, and treatments 白细胞介素-1 受体拮抗剂缺乏症：发病机制、临床特征和治疗方法的最新回顾

Clinical Immunology Communications Pub Date : 2024-09-07 DOI: 10.1016/j.clicom.2024.09.001

Spencer Fang , Joshua Pillai , Baharullah Mahin

{"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}

引用次数: 0

First report of Mycobacterium chimaera infection in a patient with chronic granulomatous disease 首次报告一名慢性肉芽肿病患者感染了奇美拉分枝杆菌

Clinical Immunology Communications Pub Date : 2024-06-23 DOI: 10.1016/j.clicom.2024.06.001

Nancy E Aguilar Gómez , Uriel Pérez Blanco , Patricia Saltigeral Simental , Sara Espinosa Padilla , Jacinta Bustamante , Lizbeth Blancas Galicia

引用次数: 0

Chronic disseminated histoplasmosis in a patient on fingolimod therapy: A case report and review of literature 芬戈莫德治疗患者的慢性播散性组织胞浆菌病：病例报告和文献综述

Clinical Immunology Communications Pub Date : 2024-06-21 DOI: 10.1016/j.clicom.2024.06.002

Aditya Sanjeevi , Brandon L Clark , Alfredo Aguirre , Basil George Verghese

引用次数: 0