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Published on: September 26, 2013
Defective signal transduction via T-cell receptor-CD3 structure in T cells from rheumatoid arthritis patients
N M Mirza1, V Relias, E J Yunis
1Division of Immunogenetics, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.
Abstract:
T cells from patients with active RA are known to produce low levels of IL-2 and proliferate poorly in response to various mitogenic stimuli. The present work shows that cross-linking of CD3 antigen on patients' T-cell surface induces two- to threefold lower Ca2+ response than in T cells from age-matched controls. Immunofluorescence studies indicate that the attenuated signal may be due to the suppressed expression of CD3 and/or CD45 molecules on patients' T cells. In the majority of the patients, the level of CD45 expression is reduced by 60%-70% as compared with that in the control T cells. Therefore, the poor mitogenic response of patient cells is apparently due to a defect in early stages of signal transduction through the T-cell receptor (TCR-CD3).
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