Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Blood. 2010 Aug 26;116(8):1263-71. doi: 10.1182/blood-2010-02-267583. Epub 2010 May 20.
Destructive midline granulomatous disease characterized by necrotizing granulomas of the head and neck is most commonly caused by Wegener granulomatosis, natural killer/T-cell lymphomas, cocaine abuse, or infections. An adolescent patient with myasthenia gravis treated with thymectomy subsequently developed extensive granulomatous destruction of midface structures, palate, nasal septum, airways, and epiglottis. His lymphocyte numbers, total immunoglobulin G level, and T-cell receptor (TCR) repertoire appeared normal. Sequencing of Recombination activating gene-1 (Rag1) showed compound heterozygous Rag1 mutations; a novel deletion with no recombinase activity and a missense mutation resulting in 50% Rag activity. His thymus was dysplastic and, although not depleted of T cells, showed a notable absence of autoimmune regulator (AIRE) and Foxp3(+) regulatory T cells. This distinct Rag-deficient phenotype characterized by immune dysregulation with granulomatous hyperinflammation and autoimmunity, with relatively normal T and B lymphocyte numbers and a diverse TCR repertoire expands the spectrum of presentation in Rag deficiency. This study was registered at www.clinicaltrials.gov as #NCT00128973.
以头颈部坏死性肉芽肿为特征的破坏性中线肉芽肿病最常见的病因是 Wegener 肉芽肿、自然杀伤/T 细胞淋巴瘤、可卡因滥用或感染。一名患有重症肌无力的青少年患者在接受胸腺切除术治疗后,出现广泛的中面部结构、 palate、鼻中隔、气道和会厌的肉芽肿性破坏。他的淋巴细胞数量、总免疫球蛋白 G 水平和 T 细胞受体(TCR)库似乎正常。重组激活基因-1(Rag1)的测序显示 Rag1 存在复合杂合突变;一种新型的无重组酶活性的缺失突变和导致 50%Rag 活性的错义突变。他的胸腺发育不良,尽管 T 细胞没有耗竭,但明显缺乏自身免疫调节因子(AIRE)和 Foxp3(+)调节性 T 细胞。这种独特的 Rag 缺陷表型的特征是免疫失调伴肉芽肿性炎症和自身免疫,相对正常的 T 和 B 淋巴细胞数量和多样化的 TCR 库扩展了 Rag 缺陷的表现谱。该研究在 www.clinicaltrials.gov 上注册为 #NCT00128973。