Clonal Silencing of Self-reactive B Lymphocytes in a Transgenic Mouse Model
- C.C. Goodnow*,
- J. Crosbie*,
- S. Adelstein*,
- T.B. Lavoie†,
- S.J. Smith-Gill†,
- D.Y. Mason§,
- H. Jorgensen*,
- R.A. Brink*,
- H. Pritchard-Briscoe*,
- M. Loughnan‡,
- R.H. Loblay*,
- R.J. Trent*, and
- A. Basten*
- *Centenary Institute of Cancer Medicine and Cell Biology, University of Sydney, New South Wales, Australia 2006; †Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892; ‡Walter and Eliza Hall Insitute, P.O. Royal Melbourne Hospital, Victoria, Australia 3050; §Nuffield Department of Pathology, John Radcliffe Hospital, Oxford, United Kingdom OX3 9DU
This extract was created in the absence of an abstract.
Excerpt
The ability of the immune system to distinguish between self-antigens and foreign antigens is a remarkable process. As a feat of developmental biology, immunological self-tolerance is all the more remarkable even when one considers the diversity of self-antigens that must be tolerated, including carbohydrates, lipids, nucleic acids, and approximately 40,000 different self-proteins, and the diversity of potentially self-reactive lymphocytes that must be tolerized. Among the possible cellular mechanisms for ensuring tolerance to self-antigens, irreversible deletion of self-reactive T lymphocytes has recently been shown to play a major role in maintaining self-tolerance within the helper and cytotoxic T-cell subsets (Kappler et al. 1987, 1988; Kisielow et al. 1988; MacDonald et al. 1988; Pullen et al. 1988; Sha et al. 1988; Davis et al., this volume). Self-tolerance in B lymphocytes expressing immunoglobulin M (IgM) antigen receptors only may also be brought about through clonal deletion of self-reactive cells (Nemazee and Bürki 1989)....
