Don Mason (immunologist)

Don Mason
Residence Oxford, UK
Citizenship British
Institutions University of Oxford
Known for Work on Regulatory T Cells

Donald W. "Don" Mason is a British immunologist and former professor of immunology in the MRC Cellular Immunology Unit at the Sir William Dunn School of Pathology at the University of Oxford. Professor Mason is best known for his work on regulatory T cells and their role in preventing autoimmunity.

Notable Work

Although Mason began life as a physicist studying nuclear fusion, he is best known for his work on cellular immunology.[1] Mason's most important contributions to immunology are his studies defining the existence, cell surface phenotype and function of regulatory T cells. Mason's studies identified the immuno-regulatory capacity of a population of CD4+ T cells which expressed low levels of OX22 (an isoform of CD45: CD45RC in rats and CD45RB in mice[2]) and their capacity to prevent the pathogenic activity of the OX22hi subset.[3] While he carried out studies into multiple sclerosis.[4], the work for which he is most recognised focused mainly on the role of Tregs in the prevention of diabetes[5] and thyroiditis[6] and highlighted the role for the thymus in the development of Tregs,.[7][8] These were among the earliest demonstrations of the requirement for Treg in restraining the pathogenic activity of CD4+ T cells and prevention of autoimmunity.[9] Prof. Mason retired from research in 1999 and still lives in the Oxford area.[10]

References

  1. ↑ Alan Frederick Williams. 25 May 1945 – 9 April 1992: Elected F.R.S. 1992 (1 December 2004)
  2. ↑ Saouid A, Seddon B, Heath V, Fowell D, Mason D (1996). "The physiological role of regulatory T cells in the prevention of autoimmunity: the function of the thymus in the generation of the regulatory T cell subset". Immunological Reviews. 149: 195–216. PMID 9005215. doi:10.1111/j.1600-065x.1996.tb00905.x.
  3. ↑ Powrie F, Mason D (1990). "OX-22high CD4+ T cells induce wasting disease with multiple organ pathology: prevention by the OX-22low subset". Journal of Experimental Medicine. 172 (6): 1701–8. PMC 2188779 Freely accessible. PMID 2258700. doi:10.1084/jem.172.6.1701.
  4. ↑ Esther M. Sternberg (2001), The Balance Within: The Science Connecting Health and Emotions, USA: Times Books, p. 97, ISBN 0-7167-4445-7
  5. ↑ Fowell D, Mason D (1993). "Evidence that the T cell repertoire of normal rats contains cells with the potential to cause diabetes. Characterization of the CD4+ T cell subset that inhibits this autoimmune potential". Journal of Experimental Medicine. 177 (3): 627–36. PMC 2190953 Freely accessible. PMID 8094734. doi:10.1084/jem.177.3.627.
  6. ↑ Seddon B, Mason D (1999). "Regulatory T cells in the control of autoimmunity: the essential role of transforming growth factor beta and interleukin 4 in the prevention of autoimmune thyroiditis in rats by peripheral CD4(+)CD45RC- cells and CD4(+)CD8(-) thymocytes". Journal of Experimental Medicine. 189 (2): 279–88. PMC 2192980 Freely accessible. PMID 9892610. doi:10.1084/jem.189.2.279.
  7. ↑ Saouid A, Seddon B, Mason D (1996). "The thymus contains a high frequency of cells that prevent autoimmune diabetes on transfer into prediabetic recipients". Journal of Experimental Medicine. 184 (6): 2393–8. PMC 2196374 Freely accessible. PMID 8976193. doi:10.1084/jem.184.6.2393.
  8. ↑ Saouid A, Seddon B, Heath V, Fowell D, Mason D (1996). "The physiological role of regulatory T cells in the prevention of autoimmunity: the function of the thymus in the generation of the regulatory T cell subset". Immunological Reviews. 149: 195–216. PMID 9005215. doi:10.1111/j.1600-065x.1996.tb00905.x.
  9. ↑ Sakaguchi S (2004). "Naturally arising CD4+ regulatory t cells for immunologic self-tolerance and negative control of immune responses". Annual Review of Immunology. 22: 531–62. PMID 15032588. doi:10.1146/annurev.immunol.21.120601.141122.
  10. ↑ Mason, Don. "The Broader View" (PDF). Fusion. University of Oxford. Retrieved 28 July 2016.
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.