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Ernesto L. Schiffrin

Ernesto L. Schiffrin, CM, MD, PhD, FRSC, FRCPC, FACP

Molecular & Regenerative Medicine

Endothelin, Endothelium, Gamma/delta T lymphocytes, Genes, Immune mechanisms, Inflammation, Renin-angiotensin-aldosterone system, Single cell sequencing, T cells, Vascular remodeling
  • Senior Investigator and Director, Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research
  • Physician-in-Chief Emeritus, Department of Medicine, Jewish General Hospital
  • Distinguished James McGill Professor and former Associate Chair, Department of Medicine, McGill University
  • Editor-in-Chief, The American Journal of Hypertension

Contact details

ernesto.schiffrin@mcgill.ca
@ESchiffrin

Assistant contact details

  • Pierre Paradis, PhD,
    Associate Director of Laboratory
    (514) 340-8222 ext. 22204
    pierre.paradis@mcgill.ca

Snapshot

Dr. Ernesto L. Schiffrin is interested in mechanisms in hypertension, particularly molecular aspects of inflammatory and immune mediators of vascular injury in hypertension, as well as treatments that can prevent vascular injury in human hypertension and improve outcomes for patients.

Important Links :

See Dr. Ernesto L. Schiffrin's publications on PubMed

Major Research Activities

Dr. Ernesto L. Schiffrin and his team have demonstrated that a subset of γδ T lymphocytes that produce IL-17A expand in perivascular adipose tissue in hypertension. γδ T cells directly activate αβ T cells which produce interferon gamma and may be final mediators in cardiovascular damage in hypertension. Development of memory γδ T cells contributes to maintenance of high BP.

 

The specific research areas in the laboratory include:

  • Currently we are testing whether depletion of specific subtypes of γδ T cells prevents BP elevation, vascular injury and T cell activation.
  • Using anti-TCRγδ depleting antibodies or adoptive transfer of γδ T cells isolated from hypertensive mice, we are verifying that memory γδ T cells develop after an initial exposure to a hypertensive stimulus and sensitize mice to develop hypertension to a subsequent subpressor hypertensive challenge.
  • We are also determining whether γδ T cells directly activate αβ T cells, and whether this is (a) enhanced by in vivo hypertensive challenges in mice or (b) whether it occurs in hypertensive humans using co-culture of murine and human γδ and αβ T cells, flow cytometry, single cell RNA sequencing (scRNA-seq) and blocking antibodies.

Recent Publications and References

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