Yoshida S H, Teuber S S, German J B, Gershwin M E
Division of Rheumatology, Allergy and Clinical Immunology, School of Medicine, University of California, Davis 95616.
Food Chem Toxicol. 1994 Nov;32(11):1089-100. doi: 10.1016/0278-6915(94)90150-3.
A variety of mechanisms can be proposed to explain the potential effects of silicone and silicone by-products on the immune response. In this paper, we discuss information on the chemistry of silicon and silicone gels/elastomers, and the manufacture of silicone breast implants as they pertain to the bioreactivity of silicone. Moreover, with reference to silicone-mediated human adjuvant disease, an overview of experimental adjuvant-induced arthritis is presented; comparisons with graft-versus-host disease and chemically induced autoimmunity then follow. Particular attention is paid to similarities in the characteristics of silicone and classic lipid adjuvants. For example, macrophage activation is presumed to be a central event in silicone-induced autoimmunity. Since those genes uniquely expressed in macrophages activated by plastic adherence are similar to those induced by lipopolysaccharide, adherence to silicone rubber may initiate an inflammatory response by the same mechanism. Macrophage effects would also include the erosion of implants through the generation of oxidants and localized pH changes. The degradation products of silicone are also implicated in the adjuvant effects of silicone implants. There is evidence to suggest that oxidants produced by inflammatory cells preferentially inactivate CD8+ suppressor T cells. This could then lead to an inflammatory state, perhaps through oxidant-induced transcription factors such as NF-kB, resulting in a long-term pro-oxidant imbalance that manifests itself as a breakdown in immunological self-tolerance. The authors hypothesize that autoreactivity following oxidant stress evolved to enhance inflammatory repair mechanisms after tissue, cell or molecular damage by oxidants.
可以提出多种机制来解释硅酮及硅酮副产物对免疫反应的潜在影响。在本文中，我们讨论了有关硅和硅胶/弹性体的化学信息，以及与硅酮生物反应性相关的硅酮乳房植入物的制造。此外，参考硅酮介导的人类佐剂病，对实验性佐剂诱导的关节炎进行了概述；随后将其与移植物抗宿主病和化学诱导的自身免疫进行比较。特别关注硅酮与经典脂质佐剂在特性上的相似之处。例如，巨噬细胞活化被认为是硅酮诱导自身免疫的核心事件。由于在通过塑料黏附活化的巨噬细胞中独特表达的那些基因与脂多糖诱导的基因相似，因此黏附到硅橡胶上可能通过相同机制引发炎症反应。巨噬细胞的作用还包括通过产生氧化剂和局部pH变化对植入物造成侵蚀。硅酮的降解产物也与硅酮植入物的佐剂作用有关。有证据表明，炎症细胞产生的氧化剂优先使CD8 +抑制性T细胞失活。这可能进而导致炎症状态，也许是通过氧化剂诱导的转录因子如NF - kB，导致长期的促氧化剂失衡，表现为免疫自我耐受的破坏。作者推测，氧化应激后的自身反应性进化而来是为了增强组织、细胞或分子受到氧化剂损伤后的炎症修复机制。
