THE ROLE OF THE INTERLEUKIN-2 (IL-2)/IL-2 RECEPTOR PATHWAY IN MRL/LPR LYMPHADENOPATHY - THE EXPANDED CD4-8- T-CELL SUBSET COMPLETELY LACKS FUNCTIONAL IL-2 RECEPTORS

Autoimmune MRL/MP-lpr/lpr (MRL/lpr) mice spontaneously develop a systemic lupus erythematosus-like disease accompanied by a profound lymphadenopathy that consists of CD4-8-B220+ alpha beta T cells. By the use of cross-linking experiments with radiolabeled interleukin-2 (IL-2), these abnormal T cells have been reported to constitutively express the IL-2 receptor beta chain (IL-2Rbeta), a signal transducing component of IL-2R, in the absence of the alpha chain (IL-2Ralpha).To critically reevaluate the role of the IL-2/IL-2R pathway in the pathogenesis of lymphadenophathy we examined expression of the IL-2Ralpha and IL-2Rbeta in MRL/lpr mice by I-125-IL-2 binding analysis and also by flow cytometric analysis using monoclonal antibodies against each component of the receptor. We found that, contrary to the previous report, the CD4-8-B220+ alpha beta T cells in lymph node (LN) of MRL/lpr mice were negative for both IL-2Ralpha and IL-2Rbeta expression. The lpr liver CD4-8-B220+ alpha beta T cells that had been implicated in the genesis of these abnormal LN T cells were also negative for IL-2Rbeta expression. Therefore, our results indicate that the IL-2/IL-2R system plays little role, if any, in the expansion of abnormal CD4-8- B220+ alpha beta T cells in MRL/lpr mice.