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

AbstractAutoimmune 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+ a P 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 β chain (IL‐2Rα), a signal transducing component of IL‐2R, in the absence of the a chain (IL‐2Rα).To critically reevaluate the role of the IL‐2/IL‐2R pathway in the pathogenesis of lymphadenophathy we examined expression of the IL‐2Rα and IL‐2Rβ in MRL/lpr mice by 125I‐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+ α β T cells in lymph node (LN) of MRL/lpr mice were negative for both IL‐2Rα and IL‐2Rβ expression. The lpr liver CD4−8−B220+ a P T cells that had been implicated in the genesis of these abnormal LN T cells were also negative for IL‐2Rβ 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+ α β T cells in MRL/lpr mice.