Transcriptional Coactivator BOB1 (OBF1, OCA-B) in Autoimmune Diseases

Abstract

Despite significant efforts in biomedicine for several decades, autoimmune diseases continue to remain largely incurable and, moreover, poorly understood in terms of the molecular mechanisms underlying their onset and progression. It is generally accepted that autoimmune pathologies result from a malfunction of the adaptive immune system in genetically susceptible individuals leading to the appearance of autoreactive B- and T-lymphocytes. However, the exact molecular pathways that drive the activation of autoreactive lymphocytes, leading to the amplification and perpetuation of self-directed immune responses are largely unknown. A number of experimental data accumulated over the past few years indicate a key role of BOB1, namely its imbalanced expression, in the onset of autoreactive lymphocytes. It has been postulated that the coactivator BOB1 affects transcription and local chromatin state indirectly, via selective interaction with DNA-binding POU-domain transcription factors – ubiquitous OCT1 and B-cell-specific OCT2, stabilises the binding of the OCT factors to DNA. The review lists the latest evidences of an important role of BOB1 in pathogenesis of autoimmune diseases and positions this protein as a promising target in the treatment of these diseases.