This historical study examines blood-derived cells and laboratory function. Its findings and first-discovery claim reflect 2004 research, not a current diagnostic test or treatment recommendation.
J Exp Med. 2004 Apr 5;199(7):971-9
Viglietta V, Baecher-Allan C, Weiner HL, Hafler DA.
Laboratory of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, 77 Ave. Louis Pasteur, Boston, MA 02115
CD4(+)CD25(+) regulatory T cells contribute to the maintenance of peripheral tolerance by active suppression because their deletion causes spontaneous autoimmune diseases in mice.
Human CD4(+) regulatory T cells expressing high levels of CD25 are suppressive in vitro and mimic the activity of murine CD4(+)CD25(+) regulatory T cells.
Multiple sclerosis (MS) is an inflammatory disease thought to be mediated by T cells recognizing myelin protein peptides.
We hypothesized that altered functions of CD4(+)CD25(hi) regulatory T cells play a role in the breakdown of immunologic self-tolerance in patients with MS.
Here, we report a significant decrease in the effector function of CD4(+)CD25(hi) regulatory T cells from peripheral blood of patients with MS as compared with healthy donors.
Differences were also apparent in single cell cloning experiments in which the cloning frequency of CD4(+)CD25(hi) T cells was significantly reduced in patients as compared with normal controls.
These data are the first to demonstrate alterations of CD4(+)CD25(hi) regulatory T cell function in patients with MS.
Source details
Author: Viglietta V, Baecher-Allan C, Weiner HL, Hafler DA.
Archive capture: . This is not a medical review date.