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Polymorphisms in genes related to the complement system and antibody-mediated cardiac allograft rejection

Grecia M Marrón-Liñares1, Lucía Núñez1, María G Crespo-Leiro2

  • 1Grupo de investigación en Cardiología, Instituto de Investigación Biomédica de A Coruña (INIBIC), Complexo Hospitalario Universitario de A Coruña (CHUAC), Servizo Galego de Saúde (SERGAS), Universidade da Coruña (UDC), A Coruña, Spain.

The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation
|August 9, 2017
PubMed

Insights

Genetic variants in complement genes, mannose-binding lectin 2 (MBL2) and properdin (CFP), are linked to antibody-mediated rejection (AMR) after heart transplantation (HT). These findings may help predict AMR risk in HT recipients.

Area of Science:

  • Immunogenetics
  • Transplantation immunology
  • Complement system biology

Background:

  • Heart transplantation (HT) is a critical treatment for end-stage heart failure.
  • Antibody-mediated rejection (AMR) is a significant post-HT complication driven by humoral responses.
  • Complement activation is a key pathway implicated in AMR-related graft damage.

Purpose of the Study:

  • To investigate genetic variations within complement pathway genes.
  • To identify associations between these genetic variants and the development of AMR post-HT.

Main Methods:

  • Next-generation sequencing of 51 complement-related genes.
  • Analysis of 46 heart transplant recipients (23 with AMR, 23 without).
  • Statistical analysis using SNPstats and R software.

Main Results:

  • Two single nucleotide polymorphisms (SNPs) showed significant association with AMR: p.Gly54Asp in MBL2 and p.Asn428(p=) in CFP.
  • Rare MBL2 allele (p.Gly54Asp) correlated with mannose-binding lectin deficiency in controls.
  • Rare CFP allele (p.Asn428(p=)) correlated with elevated properdin levels in AMR patients.

Conclusions:

  • Genetic variants in MBL2 and CFP influence the risk of AMR after heart transplantation.
  • These findings highlight the role of complement system genetic factors in AMR pathogenesis.
  • Identifying these variants may aid in predicting AMR risk in HT recipients.
Abstract

Keywords:
antibody-mediated rejectioncomplement genesheart transplantationmannose binding lectinproperdin

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