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Massimo Mangiola, PhD D(ABHI)

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Contact

Clinical Laboratory Building, Room 4032 3477 Euler Way
Pittsburgh, PA 15213
Phone: (412) 647-0462
Fax: (412) 647-6151

Assistant Professor of Pathology, Assistant Director Histocompatibility Laboratory

Education:
BA, Natural Sciences, The University of Messina, Italy; MS, Biology, The University of Messina, Italy; PhD, Clinical and Experimental Immunology, The University of Genoa, Italy

Research Area(s):

Dr. Mangiola has several years of experience in Histocompatibility and Immunogenetics. As Assistant Director of the Histocompatibility Laboratory, Dr. Mangiola provides compatibility consultations for all solid organ and bone marrow transplants. Dr. Mangiola has several years of clinical experience in the characterization of both genetic compatibility (HLA antigenic and allelic match) between patient and donor and patient’s allosensitization status (identification of HLA antibodies).

Role of HLA epitopes in solid organ and bone marrow transplantation and the role of HLA alloantibodies in rejection of solid organs

The goal of my research is to understand the mechanisms of generation of HLA donor-specific antibodies (DSA) and the mechanisms driving antibody-mediated rejection (AMR). Identification of long-term graft loss risk factors is essential for individualized precision medicine. Patients awaiting transplant are frequently transplanted with donors highly mismatched for HLA and often against DSAs. It is universally accepted that both have a negative impact on long-term survival. The classical HLA genes translate for thousands of different HLA proteins. While these molecules share a great deal of conserved region (similarities), they possess also many polymorphic regions (dissimilarities). Therefore, for any given patient and donor pair, the number of HLA amino-acid differences that the patient will be exposed to after transplant may vary significantly. Polymorphic regions capable of eliciting an immune response, including the production of antibody, are known as epitopes or eplets. Although in organ transplantation there is evidence that some epitopes are more antigenic than others, the effect of the epitope load differences between patient and donor must be studied in more detail. Epitope mismatch load may be an important tool to stratify patient-donor pairs based on the individual risk of a patient to develop DSAs, AMR or ACR (acute cellular rejection). My research focuses on a multi-variate analysis of the epitope load mismatch against several clinical and pathological post-transplant data. The differences in epitope mismatch load between transplant pairs may have strong significance as a risk stratification tool and may help create the basis for individualized treatment and surveillance of post-transplant patients.