Clinical Immunology Communications最新文献

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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

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.

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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

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.

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

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.

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

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.

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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

Anti-type-I interferon (IFN) autoantibodies have been associated with severe COVID-19. Their association with long COVID, however, is unclear.

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.

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.

抗I型干扰素（IFN）自身抗体与严重的COVID-19有关。我们对因急性COVID-19住院的患者（97人）进行了为期一年的抗IFN-α2抗体水平随访。在 5/97 例患者中检测到了特异性抗 IFN-α2 抗体。只有住进重症监护室的患者（3/42）在急性感染期间检测到高水平的抗 IFN-α2 抗体，其中 2 人在感染后 12 个月的胸部计算机断层扫描中检测到持续的高水平抗 IFN-α2 抗体和残留变化。总之，急性感染期间的抗 IFN-α2 抗体与 SARS-CoV-2 后遗症无关。两名最初检测不到抗IFN-α2自身抗体的患者在感染后12个月出现自身抗体水平升高。要研究 SARS-CoV-2 感染后耐受性丧失在长期 COVID 中的潜在作用，还需要进行更多的大型研究。

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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

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. RELA, RELB, and RELC were knocked out using CRISPR/Cas9-mediated homologous recombination in CD4⁺/CD8⁺ T cells and Tregs isolated from healthy donors. The RELA, RELB, and RELC knockouts did not alter the phenotype or cytokine production profile of CD4⁺/CD8⁺ T cells or Jurkat cells. Similar to that observed in knockout mice, RELA or RELC 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.

NF-κB 相关分子的突变会导致以反复感染为特征的联合免疫缺陷症。在这项研究中，我们旨在研究 NF-κB 家族成员 RELA、RELB 和 RELC 的突变与人类调节性 T 细胞（Treg）功能之间的关联。研究人员利用 CRISPR/Cas9 介导的同源重组技术敲除了从健康供体中分离出来的 CD4+/CD8+ T 细胞和 Tregs 中的 RELA、RELB 和 RELC。RELA、RELB和RELC基因敲除并没有改变CD4+/CD8+ T细胞或Jurkat细胞的表型或细胞因子产生情况。与在基因敲除小鼠中观察到的情况类似，MT-2细胞和新鲜分离的Tregs中的RELA或RELC基因敲除也降低了FOXP3的表达和Tregs的免疫抑制功能。此外，在敲除 RELC 后，效应 T 细胞和 Tregs 中的 PD-L1 表达也大大减少。这些研究结果表明，由于 FOXP3 表达下调，删除 RELA 或 RELC 会导致 Treg 样表型和功能的丧失。

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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

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.

白细胞介素-1受体拮抗剂缺乏症（DIRA）是一种罕见的常染色体隐性自身炎症性疾病，于2009年首次报道。迄今为止，已有 33 例患者的特征被描述出来，并有文献报道。据我们所知，近期还没有任何研究广泛评估了对这种具有挑战性且危及生命的疾病的最新认识进展。在此，我们全面回顾了 DIRA 的病因和细胞遗传学异常。然后，我们研究了目前用于识别这种疾病变异体的诊断方法。此外，我们还报告了目前患者样本中广泛存在的人口统计学特征。最后，我们讨论了患者使用的治疗方法（抗生素、皮质类固醇等）和主要生物制剂（阿纳金拉、卡纳库单抗、阿达木单抗和利龙赛普），以及有关其临床安全性和有效性的最新信息。总之，尽管这种疾病还需要进一步的研究，但这篇综述可能会对治疗和管理DIRA患者的临床医生有所启发。

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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

Chronic granulomatous disease (CGD) is an inborn error of immunity. NADPH oxidase is an enzyme complex that produces various reactive oxygen species, such as superoxide anions and hydrogen peroxide. Mycobacterial infections in CGD are commonly observed in countries with a high prevalence of these microorganisms, such as those receiving the BCG vaccination at birth or having a high prevalence of tuberculosis. Non-tuberculous mycobacteria (NTM) infections are rare in CGD. The patient also presented with hemophagocytic lymphohistiocytosis, which resolved with gammaglobulin and cyclosporine. Herein, we describe the first case of M. chimaera infection in a female patient with autosomal recessive CGD caused by a pathogenic variant in CYBA.

慢性肉芽肿病（CGD）是一种先天性免疫错误。NADPH 氧化酶是一种产生各种活性氧（如超氧阴离子和过氧化氢）的酶复合物。CGD 中的分枝杆菌感染常见于这些微生物流行率较高的国家，如出生时接种卡介苗或结核病流行率较高的国家。非结核分枝杆菌（NTM）感染在CGD中很少见。患者还伴有嗜血细胞淋巴组织细胞增多症，使用丙种球蛋白和环孢素后症状缓解。在此，我们描述了首例由CYBA致病变体引起的常染色体隐性CGD女性患者感染M.

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

We present an interesting case of a 65-year-old female patient who was taking fingolimod for relapsing-remitting multiple sclerosis. She presented with a tongue nodule, oral ulcer, and was found to have CD4 lymphocytopenia. HIV serology was negative. Fingolimod is known to cause lymphocyte redistribution to lymph nodes and was deemed to be the cause of CD4 lymphocytopenia in this patient. Further evaluation with excision biopsy of the tongue nodule confirmed histoplasmosis. Treatment with itraconazole resulted in a complete resolution of her lesions.

我们为您介绍一例有趣的病例：一名 65 岁的女性患者正在服用芬戈莫德治疗复发缓解型多发性硬化症。她出现舌结节和口腔溃疡，并发现 CD4 淋巴细胞减少。艾滋病病毒血清学检测呈阴性。芬戈莫德可导致淋巴细胞重新分布到淋巴结，因此被认为是导致该患者 CD4 淋巴细胞减少的原因。通过舌结节切除活检进行的进一步评估证实了组织胞浆菌病。使用伊曲康唑治疗后，她的病变完全消退。

引用次数: 0

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