Lack of intermediate-affinity interleukin-2 receptor in mice leads to dependence on interleukin-2 receptor alpha, beta and gamma chain expression for T cell growth

Eur J Immunol. 1996 Jan;26(1):201-6. doi: 10.1002/eji.1830260131.


An interleukin (IL)-4 dependent mouse T cell clone 8.2 derived from an IL-2-dependent T cell line was characterized. As measured by flow cytometric analysis and Northern blotting, it expresses IL-2 receptor beta (IL-2R beta) and gamma (IL-2R gamma) chains, but has lost expression of IL-2 receptor alpha chain (IL-2R alpha). To investigate the properties of the mouse IL-2R beta gamma complex and the role of IL-2R alpha gene expression, this clone was further studied. T cell clone 8.2 has lost the capacity to bind 125I-labeled human IL-2 under experimental conditions able to detect intermediate-affinity IL-2R in human cells. Mouse IL-2 is unable to block the binding of mAb TM beta 1 to 8.2 cells. Under the same experimental conditions, mouse IL-2 blocks the binding of TM beta 1 to C30-1 cells expressing the IL-2 alpha beta gamma complex. Since TM beta 1 recognizes an epitope related to the IL-2 binding site of IL-2R beta, these results can be taken as a demonstration that mouse IL-2R beta gamma does not bind mouse IL-2. Furthermore, T cell clone 8.2 does not proliferate in response to recombinant mouse or human IL-2. On the other hand, T cell transfectant lines expressing heterospecific receptors made of the human IL-2R beta and mouse IL-2R gamma chains bind 125I-labeled human IL-2 and proliferate in response to IL-2. This establishes the difference between mouse and human IL-2R beta chains. Transfection of T cell clone 8.2 with human IL-2R alpha genes restores their capacity to proliferate in response to IL-2. In addition, all transfectants grown in IL-2 express the endogeneous mouse IL-2R alpha chain. When grown in IL-4, the endogeneous mouse IL-2R alpha gene remains silent in all these transfectants. These results show that, contrary to the human, the mouse does not express an intermediate-affinity IL-2R. Expression of the IL-2R alpha gene is therefore required for the formation of the functional IL-2R in mice.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Cell Division / immunology
  • Cell Line
  • Clone Cells
  • Humans
  • Interleukin-2 / chemistry
  • Lymphocyte Activation
  • Mice
  • Protein Binding / immunology
  • Receptors, Interleukin-2 / biosynthesis*
  • Receptors, Interleukin-2 / genetics
  • Receptors, Interleukin-2 / physiology
  • T-Lymphocytes / cytology*
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism*
  • Transfection


  • Interleukin-2
  • Receptors, Interleukin-2