Donald W. Mason
University of Oxford
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Donald W. Mason.
Archive | 1980
Donald W. Mason; Roger J. Brideau; W. Robert McMaster; Michael Webb; Robert A. H. White; Alan F. Williams
All lymphocytes have the same morphological appearance, but they can be functionally split into two main categories. B lymphocytes differentiate in the bursa (avia) or bone marrow (mammalia) and give rise to antibody-secreting cells, while T lymphocytes differentiate in the thymus and are responsible for cell-mediated immunity (Moller, 1969). These differences in function and ontogeny correlate with the expression of different cell-surface molecules (antigens) on B and T lymphocytes and antibodies to these molecules have been important as markers for identifying and separating different cell types (Raff, 1971). The possibility that marker antigens have important functional roles is illustrated by the fact that cell-surface immunoglobulin (sIg) is a standard marker for B lymphocytes and is also the receptor for antigen on these cells.
Journal of Neuroimmunology | 1986
Steven W. Brostoff; Donald W. Mason
The role of lymphocyte subsets in rat EAE was investigated using a passive transfer system in which spleen cells from sensitized donors were injected into naive recipients after incubation in culture for 72 h with myelin basic protein. The presence of anti-I-A antibody, but not anti-I-E antibody during incubation, prevented disease. In addition, removal of I-A+ cells by rosetting prior to injection eliminated the ability of the donor splenocytes from transferring disease while the simultaneous removal of both cytotoxic/suppressor and B cells had no effect on the disease outcome.
Annals of the New York Academy of Sciences | 1988
Iain A.M. MacPhee; Donald W. Mason
Lewis rats immunized with myelin basic protein (MBP) in complete Freund’s adjuvant experience a single episode of paralysis and after recovery are refractory to further disease induction.’ The processes bringing about this refractory state, which may be similar to those involved in the remissions observed in multiple sclerosis, are still poorly understood. Here we examine in EAE the possible role of an immunoregulatory autoantibody found in convalescent animals. We consistently failed to adoptively transfer refractoriness to EAE with T lymphocytes, but serum from convalescent animals is a potent inhibitor of clinical signs (FIG. 1). This suppression is also seen when serum is transferred from animals immunized with whole brain homogenate in complete Freund’s adjuvant.’ Although
Journal of Neuroimmunology | 1987
Jonathan D. Sedgwick; Donald W. Mason
Previous data from our laboratory show that microglia cultured from normal mice, as well as mice infected with scrapie agent, stain with nucleoside diphosphatase, a marker of CNS mesodermal cells, and are negative for gli81 fibrillary acidic protein (Merz, et.al. Acta Neuropathol. 72:240-247, 1987). Microglia and macrophages share a number of characteristics. Our current data demonstrate the production of interleukin-I from microglia derived from both normal and scrapie infected mice. In addition to Mac-I surface marker, microglia from scrapie infected mice are positive for F4/80 antigen, a surface marker for mature macrophages.
European Journal of Immunology | 1980
Roger J. Brideau; Philip B. Carter; W. Robert McMaster; Donald W. Mason; Alan F. Williams
Nature | 1981
Donald W. Mason; M. Dallman; A. N. Barclay
European Journal of Immunology | 1991
A. J. Mcknight; A N Barclay; Donald W. Mason
European Journal of Immunology | 1982
Margaret J. Dallman; Donald W. Mason; Michael Webb
Nature | 1979
Michael Webb; Donald W. Mason; Alan F. Williams
European Journal of Immunology | 1984
Christine Bowman; Donald W. Mason; Charles D. Pusey; Christopher M. Lockwood