Complete CD16A Deficiency and Defective NK Cell Function in a Man Living with HIV.

IF 7.2 2区医学 Q1 IMMUNOLOGY

Journal of Clinical Immunology Pub Date : 2025-05-24 DOI:10.1007/s10875-025-01886-y

Weiying Zhang, Alan F Scott, David W Mohr, Roxann Ingersoll, Peter E Shoucair, Jay H Bream, Tricia L Nilles, Hao Zhang, Yue Chen, Robbie B Mailliard, Joseph B Margolick

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引用次数: 0

Abstract

A man living with HIV was found to lack expression of CD16A on his natural killer (NK) cells and monocytes. Genetic analysis revealed compound heterozygous deletion of FCGR3A, the gene encoding CD16A. The case's NK cells showed: (a) no antibody-dependent cell-mediated cytotoxicity and very low spontaneous cytotoxicity; (b) an immature phenotype marked by high expression of CD94, CD2, NKG2A, and NKG2D, and low expression of KIR2DL2 and CD57; (c) no expression of KIR3DL1 and very low expression of FcRγ; and (d) normal cytokine production. The case's monocytes and DCs were similar phenotypically and functionally to those from the donors matched for HIV status, age, and percentage of NK cells in the peripheral blood. In contrast to previously reported people with CD16A deficiency, this man did not have a history of severe infections with herpes viruses, suggesting that other immune cells and/or immunoregulatory function of NK cells may compensate for deficiency of cytolytic NK cells.

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HIV感染者完全CD16A缺失和NK细胞功能缺陷

一名HIV感染者被发现在他的自然杀伤细胞（NK）和单核细胞上缺乏CD16A的表达。遗传分析显示编码CD16A的基因FCGR3A存在复合杂合缺失。该病例的NK细胞显示：(a)无抗体依赖性细胞介导的细胞毒性和非常低的自发细胞毒性；(b)不成熟表型，CD94、CD2、NKG2A和NKG2D高表达，KIR2DL2和CD57低表达；(c) KIR3DL1不表达，FcRγ表达极低；(d)正常细胞因子的产生。该病例的单核细胞和dc在表型和功能上与HIV状态、年龄和外周血NK细胞百分比相匹配的供者相似。与先前报道的CD16A缺乏症患者相比，该患者没有严重疱疹病毒感染史，这表明其他免疫细胞和/或NK细胞的免疫调节功能可能弥补溶解NK细胞的缺陷。

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来源期刊

Journal of Clinical Immunology 医学-免疫学

CiteScore

12.20

自引率

9.90%

发文量

218

审稿时长

2 months

期刊介绍： The Journal of Clinical Immunology publishes impactful papers in the realm of human immunology, delving into the diagnosis, pathogenesis, prognosis, or treatment of human diseases. The journal places particular emphasis on primary immunodeficiencies and related diseases, encompassing inborn errors of immunity in a broad sense, their underlying genotypes, and diverse phenotypes. These phenotypes include infection, malignancy, allergy, auto-inflammation, and autoimmunity. We welcome a broad spectrum of studies in this domain, spanning genetic discovery, clinical description, immunologic assessment, diagnostic approaches, prognosis evaluation, and treatment interventions. Case reports are considered if they are genuinely original and accompanied by a concise review of the relevant medical literature, illustrating how the novel case study advances the field. The instructions to authors provide detailed guidance on the four categories of papers accepted by the journal.