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Isolation and Characterization of Adult Cardiac Fibroblasts and Myofibroblasts
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Basophils Trigger Fibroblast Activation in Cardiac Allograft Fibrosis Development.

G Schiechl1, F J Hermann1, M Rodriguez Gomez1

  • 1Department of Internal Medicine II, Nephrology, University Hospital Regensburg, Regensburg, Germany.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|March 3, 2016
PubMed
Summary

Basophils and interleukin-4 (IL-4) drive cardiac allograft fibrosis by activating fibroblasts. Targeting basophil-derived IL-4 may prevent chronic rejection and fibrotic organ remodeling.

Keywords:
basic (laboratory) research/sciencefibrosisheart (allograft) function/dysfunctionheart transplantation/cardiologyimmune regulationimmunobiologyimmunosuppression/immune modulationrejection: chronicsignaling/signaling pathways

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Area of Science:

  • Immunology
  • Transplantation Biology
  • Fibrosis Research

Background:

  • Chronic cardiac allograft rejection is characterized by significant fibrosis.
  • Resident fibroblasts are primary producers of extracellular matrix proteins in fibrosis.
  • The regulatory cells and mechanisms driving allograft fibrosis remain incompletely understood.

Purpose of the Study:

  • To investigate the role of basophils and interleukin-4 (IL-4) in regulating connective tissue production in cardiac allograft fibrosis.
  • To elucidate the cellular sources of IL-4 in the context of T-cell depleted heart transplantation.
  • To explore potential therapeutic targets for chronic allograft rejection.

Main Methods:

  • Utilized a fully MHC-mismatched heart transplantation model in mice.
  • Employed transient depletion of CD4(+) T cells to mitigate acute rejection.
  • Investigated the roles of basophils and IL-4 signaling through basophil depletion, IL-4-deficient recipients, and IL-4 receptor-deficient grafts.

Main Results:

  • Basophils and IL-4 were identified as critical mediators in the activation of fibroblasts and the development of fibrotic organ remodeling.
  • In the absence of CD4(+) T cells, basophils emerged as the predominant source of IL-4 within the cardiac allograft.
  • Basophil-derived IL-4 promoted myofibroblast expansion, interstitial collagen deposition, and the progression of allograft vasculopathy.

Conclusions:

  • Basophils play a pivotal role in initiating the production of connective tissue elements by myofibroblasts in cardiac allograft fibrosis.
  • Basophil-derived IL-4 is a key driver of fibrotic processes following heart transplantation.
  • Targeting basophil-derived IL-4 presents a promising therapeutic strategy for managing chronic allograft rejection and preventing fibrosis.