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Tolerance to liver-specific antigens.

J Forman1, K Wieties, R E Hammer

  • 1Department of Microbiology, University of Texas Southwestern Medical Center, Dallas 75235-9048.

Immunological Reviews
|August 1, 1991
PubMed
Summary
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Transgenic mice expressing Q10/L on hepatocytes achieve functional tolerance to alloreactive cytotoxic T lymphocytes (CTL). This tolerance involves the silencing of high-affinity CTL, leaving low-affinity cells unable to be primed in vivo.

Area of Science:

  • Immunology
  • Transplantation Immunology
  • T Cell Biology

Background:

  • Peripheral tolerance is crucial for preventing autoimmune diseases and transplant rejection.
  • Cytotoxic T lymphocytes (CTL) play a key role in allograft rejection.
  • Understanding mechanisms of CTL tolerance is vital for improving transplantation outcomes.

Purpose of the Study:

  • To develop and characterize a transgenic (TG) mouse model for studying peripheral tolerance of alloreactive CTL.
  • To investigate the mechanisms underlying CTL tolerance induced by hepatocyte-specific antigen expression.
  • To determine the fate and function of CTL in TG mice with antigen expression on hepatocytes.

Main Methods:

  • Generation of TG mice expressing Q10/L on hepatocytes.

Related Experiment Videos

  • In vitro and in vivo assessment of CTL numbers and function.
  • Analysis of CTL priming and activation after immunization.
  • Adoptive transfer of TG CTL into non-TG recipients.

    • Main Results:

    • TG mice expressing Q10/L on hepatocytes are functionally tolerant to alloreactive CTL.
    • Normal numbers of CTL specific for the antigen are present in TG animals in vitro.
    • Tolerance is mediated by the silencing of high-affinity CTL, with low-affinity CTL remaining.
    • Low-affinity CTL in TG mice cannot be primed in vivo and exhibit poor lytic activity in vitro.
    • These low-affinity CTL remain unprimable even after transfer to non-TG recipients, indicating inherent unresponsiveness.

    Conclusions:

    • Hepatocyte-specific expression of Q10/L induces a robust model of peripheral CTL tolerance.
    • The tolerance mechanism involves the elimination or anergy of high-affinity CTL recognizing hepatocyte-presented antigen.
    • Remaining low-affinity CTL are functionally hyporesponsive and not readily activated in vivo.
    • This form of tolerance appears stable and not easily reversible within a 10- to 17-day interval.