Sacco Keith A, Gazzin Andrea, Notarangelo Luigi D, Delmonte Ottavia M
Department of Pulmonology, Section of Allergy-Immunology, Phoenix Children's Hospital, Phoenix, AZ, United States.
Laboratory of Clinical Immunology and Microbiology, Immune Deficiency Genetics Section, National Institutes of Health, Bethesda, MD, United States.
Front Pediatr. 2023 Feb 20;11:1110115. doi: 10.3389/fped.2023.1110115. eCollection 2023.
Granulomas have been defined as inflammatory infiltrates formed by recruitment of macrophages and T cells. The three-dimensional spherical structure typically consists of a central core of tissue resident macrophages which may merge into multinucleated giant cells surrounded by T cells at the periphery. Granulomas may be triggered by infectious and non-infectious antigens. Cutaneous and visceral granulomas are common in inborn errors of immunity (IEI), particularly among patients with chronic granulomatous disease (CGD), combined immunodeficiency (CID), and common variable immunodeficiency (CVID). The estimated prevalence of granulomas in IEI ranges from 1%-4%. Infectious agents causing granulomas such Mycobacteria and Coccidioides presenting atypically may be 'sentinel' presentations for possible underlying immunodeficiency. Deep sequencing of granulomas in IEI has revealed non-classical antigens such as wild-type and RA27/3 vaccine-strain Rubella virus. Granulomas in IEI are associated with significant morbidity and mortality. The heterogeneity of granuloma presentation in IEI presents challenges for mechanistic approaches to treatment. In this review, we discuss the main infectious triggers for granulomas in IEI and the major forms of IEI presenting with 'idiopathic' non-infectious granulomas. We also discuss models to study granulomatous inflammation and the impact of deep-sequencing technology while searching for infectious triggers of granulomatous inflammation. We summarize the overarching goals of management and highlight the therapeutic options reported for specific granuloma presentations in IEI.
肉芽肿被定义为由巨噬细胞和T细胞募集形成的炎性浸润。三维球形结构通常由组织驻留巨噬细胞的中央核心组成,这些巨噬细胞可能融合形成多核巨细胞,周围是外周的T细胞。肉芽肿可能由感染性和非感染性抗原触发。皮肤和内脏肉芽肿在先天性免疫缺陷(IEI)中很常见,尤其是在慢性肉芽肿病(CGD)、联合免疫缺陷(CID)和常见变异免疫缺陷(CVID)患者中。IEI中肉芽肿的估计患病率为1%-4%。导致肉芽肿的感染因子,如非典型呈现的分枝杆菌和球孢子菌,可能是潜在免疫缺陷的“哨兵”表现。对IEI中肉芽肿的深度测序揭示了非经典抗原,如野生型和RA27/3疫苗株风疹病毒。IEI中的肉芽肿与显著的发病率和死亡率相关。IEI中肉芽肿表现的异质性给治疗的机制方法带来了挑战。在本综述中,我们讨论了IEI中肉芽肿的主要感染触发因素以及表现为“特发性”非感染性肉芽肿的主要IEI形式。我们还讨论了研究肉芽肿性炎症的模型以及深度测序技术在寻找肉芽肿性炎症的感染触发因素时的影响。我们总结了管理的总体目标,并强调了针对IEI中特定肉芽肿表现报道的治疗选择。