Dr. Abdel-Rahim A. Hamad, 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 in Sudan 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 Frontiers 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 for Pancreatic Organ Donors with Diabetes (nPOD) and appointed member of NIH HAI study section.
View complete list of publications (PubMed)
Selected Publications
- Mohamood A, Schneck J, Hamad R. Protection from autoimmune diabetes and T cell lymphoproliferation-induced by FasL mutation are differentially regulated and can be uncoupled pharmacologically. Am J Pathol 2007;171:97-106
- Xiao X, Mohamood AS, Uddin S, Gutfreund R, Nakata C, Marshall A, Kimura H, Caturegli P, Hamad AR. Inhibition of Fas ligand in NOD mice unmasks a protective role for IL-10 against insulitis development. Am J Pathol. 2011 Aug;179(2):725-32.
- Ramirez L, Hamad AAR. Status of autoimmune diabetes 20-years after the generation of BDC 2.5 islet reactive TCR transgenic mice. Invited editorial. Word J of Diabetes. 2013 Aug 15; 4(4):88-91.
- Ramirez L, Hamad AR. From non-obese diabetic to Network for the Pancreatic Organ Donor with Diabetes: New heights in type 1 diabetes research. World J Diabetes 2015 Nov 25;6(16):1309-11. doi: 10.4239/wjd.v6.i16.1309. PMID:26617973
- Saxena A, Yagita H, Donner TW, Hamad ARA. Expansion of FasL-Expressing CD5+ B Cells in Type 1 Diabetes Patients. Front Immunol. 2017 Apr 7;8:402. doi: 10.3389/fimmu.2017.00402. eCollection 2017.