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Structure and function of the interleukin 2 receptor: affinity conversion model.

A Shimizu, S Kondo, H Sabe

    Immunological Reviews
    |August 1, 1986
    PubMed
    Summary
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    Researchers identified conserved regions in human and mouse IL-2 receptors. A converter protein, crucial for IL-2 receptor function in T-cells, may explain differences in lymphoid versus non-lymphoid cells.

    Area of Science:

    • Immunology
    • Molecular Biology
    • Cell Biology

    Background:

    • The Interleukin-2 (IL-2) receptor is critical for T-cell proliferation and immune response.
    • Understanding the structural and functional differences of IL-2 receptors across cell types is essential for immune regulation.

    Purpose of the Study:

    • To clone and compare human and mouse IL-2 receptor structures.
    • To investigate the functional activity of human IL-2 receptors in different cellular contexts.
    • To elucidate the mechanism behind IL-2 receptor affinity regulation.

    Main Methods:

    • Cloning of human and mouse IL-2 receptor cDNAs.
    • Structural comparison of conserved regions.
    • Functional expression of human IL-2 receptor in a murine T-cell line (CTLL-2) via cDNA transfection.

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  • Assessment of receptor activity using monoclonal antibodies and analysis of growth signaling, affinity, and internalization.

    • Main Results:

    • Identified conserved regions in human and mouse IL-2 receptors, particularly in exons 2 and 4, and transmembrane/cytoplasmic portions.
    • Human IL-2 receptors were functionally active in murine T-cells but inactive in non-lymphoid cells.
    • Observed low affinity and aberrant internalization of IL-2 receptors in non-lymphoid cells.
    • Postulated the existence of a lymphoid-specific 'converter' protein responsible for high-affinity IL-2 receptor function.

    Conclusions:

    • Conserved regions in the IL-2 receptor likely mediate interactions with the converter protein.
    • The 'affinity conversion model' proposes that a ternary complex of IL-2, IL-2 receptor, and converter protein explains high-affinity binding.
    • The absence of the converter protein in non-lymphoid cells leads to IL-2 receptor dysfunction.