Huang, F., and Stott, D.I. (1993) Restoration of an early, progressive defect in responsiveness to T-cell activation in lupus mice by exogenous IL-2. Autoimmunity, 15(1), pp. 19-29. (doi:10.3109/08916939309004835)
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Splenic T-cells from lupus strain (NZB/W F1, Mrl/lpr) mice lack the ability to respond to concanavalin A (Con A) by secretion of IL-2 and hence expression of IL-2 receptor and proliferation. These defects were found not only in an aged group (>5 months) of mice in which obvious clinical ‘SLE like’ symptoms and elevated levels of serum autoantibodies were observed, but also in mice as young as 4-wk. We demonstrate here that the defective mitogenic activation of T-cells from lupus mice is due to the inability of T-helper cells to produce IL-2 and this defect can be restored by exogenous IL-2 in vitro. Con A-induced cell proliferation and IL-2 receptor expression on CD3+ cells from lupus mice occur only in the presence of exogenous IL-2, whereas normal T-cells from BALB/c and CBA control mice are activated by the mitogen and undergo complete cell cycling in the absence of exogenous IL-2, as they are able to secrete sufficient endogenous IL-2. The detection of impaired T-helper function in young lupus mice, before development of overt disease, and the reversible nature of the defect indicate that defective IL-2 activity may be fundamental to the mechanism of development of pathology in SLE.
|Glasgow Author(s) Enlighten ID:||Stott, Professor David|
|Authors:||Huang, F., and Stott, D.I.|
|College/School:||College of Medical Veterinary and Life Sciences|
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