Pathology Faculty Member

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  • Contact Information:

    Experimental Pathology
    101 Woodruff Circle, WMB, Suite 7301
    Atlanta, GA 30322
    404 712-2174 Phone

    For an expert Pathology consultation,
    or to send a specimen, call:

    1-404-712-5947

    Pathology Faculty Photo

    James C Zimring, MD, PhD

    Immunology
    Transfusion Medicine

    Associate Professor
    Pathology & Laboratory Medicine



    Pathology Division(s):
    Clinical Pathology
    Experimental Pathology


    Email Address:
    jzimrin@emory.edu




    Research Interests:

    - Mechanism and Translational Potential of Veto Cells
    Veto cells represent an immunoregulatory cell type that delete T cells that recognize antigens on the veto cell. Infusion of veto cells into an MHC disparate recipient results in the induction of tolerance to alloantigens on the veto cell. Thus, veto cells have potential as a therapeutic modality in transplantation. Utilizing a murine model of bone marrow transplantation, we are investigating the molecular and cellular mechanisms by which veto cells exert their effect and are investigating the potential for translating veto cell based approaches into the human transplantation setting.


    - Mechanisms of Immunization to Erythrocyte Antigens
    In the routine practice of transfusion medicine, patients often mount humoral immune responses to foreign antigens on transfused erythrocytes. There is clear evidence that erythrocyte surface antigens delivered intravenously represent a unique immune stimulus, but the mechanism by which immunization occurs is largely undetermined. We have generated a novel murine model to study the immunology of alloimmunization to RBC antigens by engineered a model antigen for which multiple tools already exist, into a blood group antigen. These studies will allow mechanistic investigations into a clinically important field that until now has been strictly limited to Human biology. Investigations include cellular and molecular mechanisms of alloimmunization to RBC antigens and immune mediated RBC destruction.