Transcriptional regulator BOB.1: Molecular mechanisms and emerging role in chronic inflammation and autoimmunity

Nataliya Yeremenko, Richard Danger, Dominique Baeten, Alexey Tomilin, Sophie Brouard

Research output: Contribution to journalReview articleAcademicpeer-review

8 Citations (Scopus)


Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation.
Original languageEnglish
Article number102833
Pages (from-to)102833
Number of pages1
JournalAutoimmunity Reviews
Issue number6
Publication statusPublished - 1 Jun 2021


  • Autoimmune diseases
  • B and T lymphocytes
  • The ternary BOB.1-OCT1-DNA complex
  • Transcriptional factor OCT1
  • Transcriptional regulator BOB.1

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