Editorial: The Role of Optineurin in Immunity and Immune-Mediated Diseases.
The multifunctional adaptor optineurin has been implicated in an increasing number of protein-protein interactions and cellular functions ever since its first identification as a binding partner for an adenoviral protein (1). Most—if not all—optineurin functions require its ubiquitin-binding domain in its C-terminus, which binds to K63- and/or M1-polyubiquinated proteins, allowing it to act, for example, as an adaptor during inflammatory signaling, autophagy, and vesicle trafficking (2–4). The interest in optineurin intensified after the identification of various mutations and polymorphisms in several human diseases, including primary open-angle glaucoma, amyotrophic lateral sclerosis (ALS), Paget's disease of the bone, and Crohn's disease. With their distinct yet unresolved pathogenesis, and complex genetic and environmental risk factors, these diseases seem unrelated at first. ALS, glaucoma, or Paget's disease are not traditionally regarded as immune-mediated diseases; however, the emerging evidence pinpoints immune system disfunction as their common denominator (5, 6). The aim of this Research Topic was to explore the role(s) of optineurin on a host of diverse cellular pathways that are directly or indirectly linked to the immune response. The articles cover immune signaling, cell death, membrane trafficking, autophagy of intracellular bacteria (xenophagy), damaged mitochondria (mitophagy), and protein aggregates.
Medical Research Council (MR/S007776/1)
Medical Research Council (MR/K000888/1)
Medical Research Council (MR/N000048/1)