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Professor Rizgar Mageed

Rizgar

Professor of Experimental Immunology

Centre: Experimental Medicine and Rheumatology

Email: r.a.mageed@qmul.ac.uk
Telephone: +44(0) 20 7882 3989

Profile

ORCID iD: 0000-0003-1561-784X

Rizgar Mageed first qualified from the College of Pharmacy at Baghdad University in 1976. He was awarded his PhD at the Royal London Hospital Medical School, London University in 1985. He was appointed Research Fellow at the Department of Immunology University of Birmingham Medical School in 1984 where he worked until 1990 and then joined the Kennedy Institute of Rheumatology as a Senior Scientist. In 1996, Rizgar was appointed Senior Lecturer at Imperial College. In 2000, Rizgar was awarded Arthritis Research-UK Fellowship and appointed Senior Lecturer at the Centre for Rheumatology at University College London. Rizgar joined Queen Mary University of London in May 2003. In 2009 Rizgar become a fellow of the Royal College of Pathologists (FRCPath) and in 2014 was awarded his fellowship by the Royal College of Physicians (FRCP).

Research

Group members

  • Research fellows: Dr. T. E. Taher; Dr. J. Bystrom
  • PhD students: Miss N. Nordin; Mr. M. Albogami; Mr. H. Muhammad; Dr. G. Mittal

Bone and Joint Research Unit

Our studies are focused on defining the molecular basis of humoral autoimmunity in patients with rheumatic diseases. These studies explore how abnormalities in intracellular signaling pathways in lymphocytes promote hyperactivity and autoimmunity. Recent studies have identified defects in key intracellular pathways in B-lymphocytes in patients with systemic lupus erythematosus (SLE). These studies showed enhanced activation of signaling pathways linked with the B-cell receptor (BCR) and the PI-3 kinase. The effect of treating SLE patients with B-lymphocyte depleting antibodies on signaling defects is also being examined. Other studies examine how biological anti-TNF? therapies modulate the immune system in patients with rheumatoid arthritis (RA). These studies show that treatment with biological anti-TNF? agents influence humoral and cellular immunity and promote the expansion of T-helper 17 (TH17) lymphocytes. Excess activation of TH17 cells results in incomplete responsiveness of patients to anti-TNF? therapy. Most recent experiments aim to explore these discoveries to develop therapies that selectively target proteins and signaling pathways in lymphocytes from patients with autoimmune diseases. In this regard, we have developed and are assessing recombinant single chain variable regions (scFv) of antibodies and small molecular inhibitors to deliver inhibitors of defective signaling pathways.

B-lymphocytes in patients with SLE have reduced level of signalling molecules that help regulate cellular functions. (A) Confocal microscopy depicting reduced Lyn level and translocation to lipid raft signalling microdomains in SLE B-lymphocytes compared with a healthy individual. Translocation of Lyn (green) into lipid raft microdomains (red) is indicated by yellow patches from merging the green and red colours. The abnormality in Lyn expression is associated with increased CD45 translocation to lipid raft signalling microdomains (B). Other molecules that partake in regulating Lyn, such as Csk (C), and c-Cbl (D) are not affected. [Scale bar in red lines= 5µm). Quantification of signalling molecule translocation shows an inverse relationship between Lyn and CD45 (E and F).

Publications

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Sponsors

 

Collaborators

Internal

  • A. S. Jawad (Rheumatology)
  • David Perrett (WHRI)
  • P. Wang (Blizard Institute)

External

  • D. Isenberg (UCL)
  • R. Jefferis (Birmingham)
  • P. Taylor (Oxford)
  • R. O. Williams (Oxford)
  • S. Gibbons (UCL)
  • P. Youinou (Brest, France)
  • Y. Renaudineau (Brest, France)
  • K. Thompson (Oslo, Norway)
  • N. Chiorazzi (New York, USA)
  • D. Capra (Oklahoma, USA)
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