Kotwal G J
Department of Microbiology and Immunology, University of Louisville School of Medicine, Kentucky 40292, USA.
J Leukoc Biol. 1997 Oct;62(4):415-29. doi: 10.1002/jlb.62.4.415.
Microorganisms interact with the immune system in multiple ways. In an interaction between a microorganism and its host, the defense of the host does not go unchallenged. Microorganisms have for decades been suspected of possessing the capabilities of hiding from and escaping the consequences of immune surveillance. Escape mechanisms like antigenic variation, latency, and genomic integration can best be described as passive mechanisms for avoiding interaction with the host immune system, to differentiate them from the more engaging and host-directed active mechanisms of interaction. Studies of the mechanism of direct entry of viruses (HIV, measles, and enteroviruses), bacteria (streptococci and staphylococci), and parasites (Leishmania and plasmodium) into immune cells like CD4+ T cells or macrophages, as reported very recently, indicate an even more aggressive mode of interaction. This aggressive mechanism of interaction with the components of the host immune system allows the microbe not only to block the normal function of immune components on the surface of immune cells from functioning, but also to obliterate a vital immune function, cellular immunity, causing immunosuppression, e.g. the depletion of CD4+ T cells due to the entry and replication of HIV. Collectively, microorganisms have evolved various mechanisms by which they can actively block almost any cellular, humoral, or systemic immune response. One general feature of the proteins that assist microorganism to immunomodulate and actively evade host defense is their structural and therefore functional similarity to the host proteins, which they effectively mimic. Understanding the different mechanisms by which microorganisms interact with the immune system can impact the design of live vaccines as well as the development of novel therapeutic immunomodulators that can provide medicine with powerful new tools to manage immune disorders, allograft rejection, remote multiple organ failure resulting from trauma, autoimmune diseases, etc.
微生物与免疫系统以多种方式相互作用。在微生物与其宿主的相互作用中，宿主的防御并非毫无挑战。几十年来，人们一直怀疑微生物具有躲避免疫监视并逃避其后果的能力。抗原变异、潜伏和基因组整合等逃逸机制，最好被描述为避免与宿主免疫系统相互作用的被动机制，以便将它们与更具参与性且针对宿主的主动相互作用机制区分开来。最近的报道表明，病毒（如艾滋病毒、麻疹病毒和肠道病毒）、细菌（如链球菌和葡萄球菌）以及寄生虫（如利什曼原虫和疟原虫）直接进入免疫细胞（如CD4 + T细胞或巨噬细胞）的机制，显示出一种更具侵袭性的相互作用模式。这种与宿主免疫系统成分的侵袭性相互作用机制，不仅使微生物能够阻止免疫细胞表面免疫成分的正常功能发挥作用，还能消除一种至关重要的免疫功能——细胞免疫，导致免疫抑制，例如由于艾滋病毒的进入和复制导致CD4 + T细胞耗竭。总的来说，微生物已经进化出各种机制，通过这些机制它们可以积极地阻断几乎任何细胞、体液或全身免疫反应。协助微生物进行免疫调节并积极逃避宿主防御的蛋白质的一个普遍特征是，它们在结构上与宿主蛋白质相似，因此在功能上也相似，它们有效地模仿了宿主蛋白质。了解微生物与免疫系统相互作用的不同机制，会影响活疫苗的设计以及新型治疗性免疫调节剂的开发，这些免疫调节剂可为医学提供强大的新工具，以管理免疫紊乱、同种异体移植排斥、创伤导致的远程多器官衰竭、自身免疫性疾病等。
