Professor Claudia Mauri, PhD

Professor Claudia Mauri, PhD

University College London
United Kingdom

Claudia Mauri is Professor of Immunology and Vice-Dean of the International Faculty of Medical Science, University College, London. She received her Doctor of Biology with magna cum laude in 1989 and PhD equivalent in 1996 from the University La Sapienza in Rome, Italy. She did postdoctoral work in London at The Kennedy Institute of Rheumatology, Imperial College, UK. She moved to University College London in 2002 where she established her group.

Professor Mauri’s main research interest lies in understanding the mechanisms driving autoimmunity, with a particular interest in understanding the function of regulatory cells in experimental models of rheumatic disease and in patients with systemic lupus erythematosus and rheumatoid arthritis.
Her group was amongst the first to identify a novel subset of B cells with a powerful immuno-suppressive capacity. Her work was seminal in the identification of CD40 activation for regulatory B-cell activation and how the adoptive transfer of this B-cell subset can efficiently prevent disease development and ameliorate established arthritis. More recently, she has shown that inflammation itself seems to be the primary requisite for Breg development. In arthritis, the inflammatory process is controlled by the gut-microflora, which promotes the differentiation of Bregs in lymphoid organs. Drastic alteration in the inflammatory process imposed by changes in the gut microbiome, either by antibiotic treatment or changes in the sterility of housing conditions, leads to a reduction in the production of IL-1β and IL-6, and concurrently in the number and functional capacity of Bregs.

Professor Mauri’s group has also translated the results obtained from experimental models to healthy individuals. She demonstrated that, in healthy individuals, Bregs can directly suppress both pro-inflammatory cytokine production by, and proliferation of, naïve, memory and auto-reactive T cells, whilst supporting the differentiation of regulatory T cells via the release of IL-10. However, in autoimmune diseases such as rheumatoid arthritis or systemic lupus erythematosus, Bregs have lost their capacity to suppress pro-inflammatory T-cell responses.

Disclosures

None

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