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Abdel-Rahim A. Hamad, M.V.Sc., Ph.D.

Photo of Dr. Abdel-Rahim A. Hamad, M.V.Sc., Ph.D.

Associate Professor of Pathology

Research Interests: Type 1 diabetes; NKT cells; DN T cells; Obesity

Background

Dr. Abdel R Hamad, B.V.Sc, M.V.Sc, Ph.D, is an Associate Professor of Pathology and Medicine. Dr. Hamad earned his B.V.Sc and M.V.Sc in veterinary medicine from the University of Khartoum and his Ph.D in immunology from the University of Colorado Health Science Center. He completed his postdoctoral training here at Johns Hopkins University School of Medicine and joined the Faculty in 2002. Dr. Hamad’s research has been continuously funded by the NIH and by private funding societies.

Dr. Hamad's research is focused on understanding pathophysiological roles of non-conventional immune lymphocytes in the regulation of autoimmunity, particularly type 1 diabetes (T1D), obesity and type 2 diabetes. He is also actively studying the role of non-conventional T cells in the regulation of immune responses to ischemia reperfusion injury (IRI).

Currently, Dr. Hamad is working along with Dr. Thomas Donner, Director of Diabetes at Johns Hopkins Hospital to translate these findings into strategies to better identify and protect individuals at risk for developing T1D. Along the way, they identified a subset of B cells that expresses Fas ligand and appears to be significantly increased in T1D patients and to cause insulitis in animal models.

In addition, Dr. Hamad is collaborating with Dr. Hamid Rabb to understand the role of a unique population of T cells that we discovered and, based our data, appear to play critical roles in the prevention of ischemia reperfusion injury (IRI), a major cause of death of kidney transplant recipients.

Dr. Hamad and his colleagues have discovered that syndecan 1 (sdc1), a heparan sulfate proteoglycan, is a specific marker of a subset of natural killer T cells (NKT) that produces IL-17 and resides exclusively in visceral adipose tissues. Deletion of sdc1 significantly reduces body fat and improves glucose tolerance in mice. Currently, Dr. Hamad and his colleagues are investigating the underlying mechanisms and finding ways to translate these findings into therapeutic for obesity.

Dr. Hamad has coauthored over 40 peer-reviewed publications and a book chapter in the fields of autoimmune diabetes, immune homeostasis and regulation. Dr. Hamad is a member of the editorial board of World Journal of Diabetes and Topic editor for Frontier in Immunology. He is also active in federal government advisory committees. He is an appointed member of HAI study section and served as ad hoc reviewer for several NIH study sections and for the European Research Council. He is also a member of American Association of Immunologists and B cell working group of the JDRF Network of Pancreatic Organ donor (nPOD) and Appointed member of NIH HAI study section.

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Titles

  • Associate Professor of Pathology
  • Associate Professor of Medicine

Departments / Divisions

Education

Degrees

  • M.V.Sc., University of Khartoum - Fac of Medicine - Khartoum - (Sudan) (1987)
  • Ph.D., University of Colorado Health Science Center (Colorado) (1996)

Research & Publications

Selected Publications

View all on Pubmed

Donner, T., S. Uddin, K. Arkara, Abdel Rahim Hamad. Potentials of FasL ligand (apoptosis inducing -molecule) as a unconventional therapeutic target in type 1 diabetes. Front Immunol. 2012; 3:196. doi: 10.3389/fimmu.2012.00196. Epub 2012 Jul 12

Martina MN, Noel S, Saxena A, Rabb H, Hamad AR. Double Negative (DN) αβ T Cells: Misperception and overdue recognition. Immunol Cell Biol. 93:305-10. 2015. PMID: 25420721

Saxena A, Khosraviani S, Noel S, Mohan D, Donner T, Hamad AR. Interleukin-10 paradox: A potent immunoregulatory cytokine that has been difficult to harness for immunotherapy. Cytokine 74(1):27-34. 2015. PMID: 25481648

Fousteri G, Ippolito E, Ahmed R, Hamad AR. Beta-cell specific autoantibodies: Are they just an indicator of type 1 diabetes? Curr Diabetes Rev. 2016. PMID: 27117244

AK Jaiswal, M Sadasivam, ARA Hamad. Syndecan-1-coating of interleukin-17-producing natural killer T cells provides a specific method for their visualization and analysis. World Journal of Diabetes 8 (4), 130. 2017. PMID: 28465789. PMCID: PMC5394732

Academic Affiliations & Courses

Graduate Program Affiliation

  • Immunology Training program
  • Pediatric training program
  • Pathobiology graduate program

Courses and Syllabi

  • Pathology and Disease Mechanisms (PDM)
  • Immunology Core Course

Activities & Honors

Memberships

  • American Association of Immunologists (AAI), 1997

    The American Association of Immunologists is an association of professionally trained scientists from all over the world dedicated to advancing the knowledge of immunology and its related disciplines, fostering the interchange of ideas and information among investigators, and addressing the potential integration of immunologic principles into clinical practice.

    The American Association of Immunologists serves its members by providing a center for the dissemination of information relevant to the field and its practices, such as educational and professional opportunities, scientific meetings, membership-derived issues and opinions, and important social and political issues.

  • JDRF/ Network of Pancreatic Organ Donor (nPOD), 2011
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    Mission

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    Type 1 diabetes, also known as ‘juvenile diabetes’, results from a self-destructive immune response against the insulin producing pancreatic beta cells. As a result of this so-called ‘autoimmune’ disease, patients with type 1 diabetes develop a life long dependence on insulin replacement therapy. Unfortunately, this form of treatment is often insufficient for preventing a number of debilitating complications including heart disease, blindness, and kidney disease, among others. As a result, JDRF is committed to finding a method for preventing or permanently reversing this disorder; an effort that would undoubtedly benefit from an improved understanding of how type 1 diabetes develops.

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    Somewhat surprisingly, many of our current concepts as to how type 1 diabetes develops result from autopsy based studies of human pancreas dating back to the 1960s (which indicated patients with this disorder had white blood cell infiltration of pancreatic islets … a condition termed ‘insulitis’), and more recently, from investigations of pancreatic material obtained from rodent models for the disease. Thanks to improved research tools, more recent autopsy studies of pancreata obtained from a limited number of individuals with type 1 diabetes have, however, challenged longstanding dogmas of how type 1 diabetes develops. Based on this need, JDRF organized and developed nPOD; the Network for Pancreatic Organ donors with Diabetes.

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    The goals of the nPOD initiative are to:

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    • Maintain a network of procuring and characterizing, in a collaborative manner, pancreata and related tissues (spleen, lymph node, pancreatic lymph node, peripheral blood, thymus and bone marrow) from cadaveric organ donors with type 1 diabetes as well as those whom are islet autoantibody positive.
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    • Utilizing these tissues, investigators will work together to address key immunological, histological, viral, and metabolic questions related to how type 1 diabetes develops.
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