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A cell-type specific CD1d expression program modulates invariant NKT cell development and function.

Michael I Zimmer1, Angela Colmone, Kyrie Felio

  • 1Department of Pathology, University of Chicago, Chicago, IL 60637, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|January 21, 2006
PubMed
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Altering CD1d expression in T cells changes invariant NK T (iNKT) cell development and function. These iNKT cells become hyporesponsive and cause liver pathology, revealing CD1d

Area of Science:

  • Immunology
  • Cellular Biology
  • T Cell Biology

Background:

  • Invariant NK T (iNKT) cells are crucial immune regulators, coordinating responses through cytokine production.
  • Mechanisms controlling iNKT cell response quality are not fully understood.
  • CD1d expression patterns are investigated for their role in regulating iNKT cell function.

Purpose of the Study:

  • To investigate if altered CD1d expression impacts iNKT cell development and function.
  • To generate and analyze a transgenic mouse model with high CD1d expression in T cells.

Main Methods:

  • Generation of Lck-CD1d transgenic (Tg+) mice with high CD1d expression on thymocytes and peripheral T cells.
  • Assessment of iNKT cell development and subset proportions in Tg+ mice.

Related Experiment Videos

  • Evaluation of iNKT cell responsiveness to antigenic stimulation in vivo.
  • Monitoring for liver pathology in Tg+ mice.

    • Main Results:

    • T cell-specific CD1d expression rescued iNKT cell development in CD1d-deficient mice.
    • Tg+ mice exhibited altered iNKT cell subset proportions compared to wild-type mice.
    • iNKT cells in Tg+ mice were hyporesponsive to antigenic stimulation.
    • Lck-CD1d Tg+ mice spontaneously developed liver pathology.

    Conclusions:

    • Altered CD1d expression programs significantly modulate iNKT cell development.
    • High CD1d expression on T cells leads to functional impairment and autoimmune-like liver pathology.
    • CD1d expression patterns are critical regulators of iNKT cell homeostasis and function.