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

Eur J Immunol. 1993 Jun;23(6):1378-80. doi: 10.1002/eji.1830230629.

Abstract

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-2R beta), a signal transducing component of IL-2R, in the absence of the alpha chain (IL-2R alpha). To critically reevaluate the role of the IL-2/IL-2R pathway in the pathogenesis of lymphadenopathy we examined expression of the IL-2R alpha and IL-2R beta 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+ alpha beta T cells in lymph node (LN) of MRL/lpr mice were negative for both IL-2R alpha and IL-2R beta 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-2R beta 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.

MeSH terms

  • Animals
  • Antigens, Surface / metabolism
  • Flow Cytometry
  • Immunoblastic Lymphadenopathy / metabolism*
  • Interleukin-2 / metabolism*
  • Leukocyte Common Antigens
  • Lymph Nodes / cytology
  • Mice
  • Mice, Mutant Strains
  • Receptors, Interleukin-2 / metabolism*
  • T-Lymphocyte Subsets / immunology*

Substances

  • Antigens, Surface
  • Interleukin-2
  • Receptors, Interleukin-2
  • Leukocyte Common Antigens