Innsbruck, Austria From the Department of Plastic and Reconstructive Surgery, the Laboratory of Autoimmunity, Division of Experimental Pathophysiology and Immunology, Biocenter, and the Institute for Legal Medicine, Innsbruck Medical University; and Excellentbeauty.
Plast Reconstr Surg. 2012 Feb;129(2):327e-337e. doi: 10.1097/PRS.0b013e31823aeacf.
The authors investigated the immunological mechanisms underlying extensive peri-silicone implant capsule formation, one of the most frequent postoperative complications in patients receiving silicone mammary implants.
The authors studied immune response activation by phenotypic and functional characterization of lymphocytes accumulated within this tissue. Intracapsular lymphoid cells and autologous peripheral blood mononuclear cells were isolated and analyzed by flow cytometry. The proportion of T regulatory cells (CD4+ CD25(high) Foxp3+ CD127), the cytokine profiles, and the T cell receptor repertoire of these cells were examined. Intracapsular T regulatory cells were then further analyzed by immunohistochemistry and functional suppression assays.
In comparison with peripheral blood, the cellular composition of intracapsular lymphocytes showed a predominance of CD4+ cells. Intracapsular T cells predominantly produced interleukin-17, interleukin-6, interleukin-8, transforming growth factor-β1, and interferon-γ, suggesting a TH1/TH17-weighted local immune response. Intracapsular T cells displayed a restricted T cell receptor α/β repertoire. The intact suppressive potential of T regulatory cells was demonstrated in crossover experiments with activated peripheral T cells. They did not, however, suppress intracapsular T cells. Interestingly, ratios of intracapsular T regulatory cells were inversely proportional to the clinical degree of capsular fibrosis.
The authors' results indicate that silicone implants trigger a specific, antigen-driven local immune response through activated TH1/TH17 cells, suggesting that ensuing fibrosis is promoted by the production of profibrotic cytokines as a consequence of faltering function of local T regulatory cells.
作者研究了导致广泛硅酮植入物周围胶囊形成的免疫学机制，这是接受硅酮乳房植入物的患者最常见的术后并发症之一。
作者通过对该组织内积聚的淋巴细胞进行表型和功能特征分析，研究了免疫反应的激活。分离并通过流式细胞术分析囊内淋巴细胞和自体外周血单核细胞。检查 T 调节细胞（CD4+ CD25(high) Foxp3+ CD127）的比例、细胞因子谱和这些细胞的 T 细胞受体库。然后通过免疫组织化学和功能抑制试验进一步分析囊内 T 调节细胞。
与外周血相比，囊内淋巴细胞的细胞组成表现出 CD4+细胞的优势。囊内 T 细胞主要产生白细胞介素-17、白细胞介素-6、白细胞介素-8、转化生长因子-β1 和干扰素-γ，提示存在 TH1/TH17 加权的局部免疫反应。囊内 T 细胞显示出受限的 T 细胞受体 α/β库。在与激活的外周 T 细胞的交叉实验中，证明了 T 调节细胞的完整抑制潜力。然而，它们并没有抑制囊内 T 细胞。有趣的是，囊内 T 调节细胞的比例与胶囊纤维化的临床程度呈反比。
作者的结果表明，硅酮植入物通过激活的 TH1/TH17 细胞触发特定的抗原驱动的局部免疫反应，提示随之而来的纤维化是由于局部 T 调节细胞功能失调导致促纤维化细胞因子的产生而促进的。
