Mon Health Medical Center, Department of Pathology, Morgantown, WV, USA.
Department of Surgery, Advocate Lutheran General Hospital & University of Illinois School of Medicine, Park Ridge, IL, USA.
Autoimmun Rev. 2022 Oct;21(10):103164. doi: 10.1016/j.autrev.2022.103164. Epub 2022 Aug 2.
Abdominal aortic aneurism (AAA) is a complex immunological disease with a strong genetic component, and one of the ten leading causes of death of individuals 55-74 years old worldwide. Strong evidence has been accumulated suggesting that AAA is an autoimmune specific antigen-driven disease. Mononuclear cells infiltrating AAA lesions comprised of T and B lymphocytes and other cells expressing early-, intermediate- and late-activation antigens, and the presence of antigen-presenting cells have been documented, demonstrating an ongoing immune response. The three components of the trimolecular complex, T-cell receptor (TCR)/peptide (antigen)/HLA have been identified in AAA, and specifically: (i) clonal expansions of T-cell clones in AAA lesions; (ii) the association of AAA with particular HLA Class I and Class II; and (iii) self or nonself putative AAA-associated antigens. IgG autoantibodies recognizing proteins present in normal aortic tissue have been reported in patients with AAA. Molecular mimicry, defined as the sharing of antigenic epitopes between microorganisms (bacteria, viruses) and self antigens, maybe is responsible for T-cell responses and antibody production in AAA. Also, the frequency and the suppressor activity of CD4+ CD25+ FOXP3+ Tregs and the expression of FOXP3 transcripts and protein have been reported to be significantly impaired in AAA patients vs normal donors.
腹主动脉瘤（AAA）是一种具有强烈遗传成分的复杂免疫性疾病，也是全球 55-74 岁人群十大死亡原因之一。大量证据表明，AAA 是一种自身免疫性特定抗原驱动的疾病。已经有文献记录了浸润在 AAA 病变中的单核细胞，其中包括 T 和 B 淋巴细胞以及表达早期、中期和晚期激活抗原的其他细胞，并且存在抗原呈递细胞，这表明存在持续的免疫反应。在 AAA 中已经鉴定出三分子复合物的三个组成部分，即 T 细胞受体（TCR）/肽（抗原）/HLA，具体为：（i）AAA 病变中 T 细胞克隆的克隆扩增；（ii）AAA 与特定 HLA Ⅰ类和Ⅱ类的关联；和（iii）自身或非自身假定的 AAA 相关抗原。已经在 AAA 患者中报告了识别正常主动脉组织中存在的蛋白质的 IgG 自身抗体。分子模拟，定义为微生物（细菌、病毒）和自身抗原之间抗原表位的共享，可能是导致 AAA 中 T 细胞反应和抗体产生的原因。此外，与正常供体相比，AAA 患者的 CD4+CD25+FOXP3+Treg 的频率和抑制活性以及 FOXP3 转录本和蛋白的表达已经被报道显著受损。
