Abstract

The tumour necrosis factor (TNF) family members B cell activating factor (BAFF) and APRIL (a proliferation-inducing ligand) are crucial survival factors for peripheral B cells. An excess of BAFF leads to the development of autoimmune disorders in animal models, and high levels of BAFF have been detected in the serum of patients with various autoimmune conditions. In this Review, we consider the possibility that in mice autoimmunity induced by BAFF is linked to T cell-independent B cell activation rather than to a severe breakdown of B cell tolerance. We also outline the mechanisms of BAFF signalling, the impact of ligand oligomerization on receptor activation and the progress of BAFF-depleting agents in the clinical setting.

Author affiliations

1. Department of Immunology, Faculty of Medicine, Nursing and Health Sciences, Monash University, Alfred Hospital, 86 Commercial Road, Melbourne, Victoria 3004, Australia.
2. Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, Epalinges, CH-1066, Switzerland.

Correspondence to: Fabienne Mackay¹ Email: f.mackay@med.monash.edu.au

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