Holers V Michael, Tomlinson Stephen, Kulik Liudmila, Atkinson Carl, Rohrer Bärbel, Banda Nirmal, Thurman Joshua M
Departments of Medicine and Immunology, University of Colorado School of Medicine, Aurora, CO, United States.
Research Service, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC, United States; Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, United States.
Semin Immunol. 2016 Jun;28(3):260-7. doi: 10.1016/j.smim.2016.05.007. Epub 2016 Jun 6.
Despite substantial opportunity and commercial interest in developing drugs that modulate the complement system in a broad range of non-orphan indications, several obstacles remain to be overcome. Among these issues is the biophysical nature of complement proteins, whose circulating levels are typically very high and whose turnover rates are relatively rapid, especially in the setting of chronic inflammatory conditions. This situation necessitates the use of very high levels of therapeutic compounds in order to achieve both multi-pathway and multiple effector mechanism inhibition. In addition, one must avoid infectious complications or the systemic impairment of the other important physiological functions of complement. Herein we focus on the development of a novel therapeutic strategy based on injured tissue-specific targeting of complement inhibitors using the antigen-combining domains of a small subset of natural IgM antibodies, which as endogenous antibodies specifically recognize sites of local damage across a broad range of tissues and locally activate complement C3, resulting in C3 fragment covalent fixation. Because the use of such recombinant tissue-targeting inhibitors precludes the utility of measuring systemic levels of complement biomarkers or function, since a goal of this targeting strategy is to leave those processes intact and unimpeded, we also briefly describe a new method designed to quantitatively measure using imaging modalities the inhibition of generation of fixed C3 fragments at sites of inflammation/injury. In addition to the ability to determine whether complement activation is locally constrained with the use of inhibitors, there is also a broader application of this imaging approach to inflammatory and autoimmune diseases characterized by local complement activation.
尽管在开发用于多种非罕见适应症的调节补体系统的药物方面存在大量机会和商业利益,但仍有几个障碍有待克服。这些问题包括补体蛋白的生物物理性质,其循环水平通常非常高,周转率相对较快,尤其是在慢性炎症情况下。这种情况需要使用非常高剂量的治疗化合物,以实现多途径和多效应器机制的抑制。此外,必须避免感染并发症或补体其他重要生理功能的全身性损害。在此,我们专注于开发一种新的治疗策略,该策略基于使用一小部分天然IgM抗体的抗原结合域对补体抑制剂进行损伤组织特异性靶向,这些天然IgM抗体作为内源性抗体可特异性识别广泛组织中的局部损伤部位并局部激活补体C3,从而导致C3片段共价固定。由于使用这种重组组织靶向抑制剂排除了测量补体生物标志物或功能的全身水平的效用,因为这种靶向策略的目标是使这些过程保持完整且不受阻碍,我们还简要描述了一种新方法,该方法旨在使用成像方式定量测量炎症/损伤部位固定C3片段生成的抑制情况。除了能够确定使用抑制剂时补体激活是否受到局部限制外,这种成像方法在以局部补体激活为特征的炎症和自身免疫性疾病中也有更广泛的应用。