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Related Experiment Video

Updated: Mar 28, 2026

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Protein Quantitative Trait Loci Analysis Identifies Genetic Variation in the Innate Immune Regulator TOLLIP in

E Cantu1, Y Suzuki1, J M Diamond2

  • 1Division of Cardiovascular Surgery, University of Pennsylvania School of Medicine, Philadelphia, PA.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|December 15, 2015
PubMed
Summary

Genetic analysis identified a link between Toll interacting protein (TOLLIP) variants and primary graft dysfunction (PGD). This finding supports TOLLIP

Keywords:
dysfunctionimmuneinflammatoryischemia reperfusion injury (IRI)lung (allograft) functionlung diseaselung transplantationpulmonologysciencetranslational research

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Area of Science:

  • Immunology
  • Genetics
  • Pulmonary Medicine

Background:

  • Plasma plasminogen activator inhibitor-1 (PAI-1) is a known biomarker for primary graft dysfunction (PGD).
  • Identifying genetic factors influencing PAI-1 levels can elucidate PGD pathogenesis.

Purpose of the Study:

  • To investigate if plasma PAI-1 levels as a quantitative trait can help discover genetic loci associated with PGD.
  • To determine the role of genetic variations in PGD development.

Main Methods:

  • A two-stage cohort study design was employed.
  • Stage 1 involved linear modeling to associate genetic loci with plasma PAI-1 levels in 297 individuals.
  • Stage 2 tested significant loci for association with PGD in 728 patients.

Main Results:

  • Six loci associated with PAI-1 were identified in Stage 1.
  • The rs3168046 variant in the Toll interacting protein (TOLLIP) gene was significantly associated with PGD (p=0.006).
  • Carrying at least one copy of rs3168046 increased PGD risk by 11.7%.

Conclusions:

  • Genetic variants in the TOLLIP gene are linked to higher PAI-1 plasma levels and clinical PGD.
  • This study validates the association of TOLLIP variants with PGD.
  • The findings suggest a role for Toll-like receptors in PGD pathogenesis.