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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

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 and joined the Faculty in 2002. He is a member of American Association of Immunologists and B cell working group of the Network of Pancreatic Organ donor (nPOD). Hamad’s research on autoimmunity and T cells has been continuously funded by the NIH at the R01 level and by private funding societies.

Dr. Hamad research is focused on understanding pathophysiological roles of non-conventional immune lymphocytes in the regulation of autoimmunity, particularly type 1 diabetes, 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). Dr. Hamad interest in these apparently disparate studies is commonly linked and branched from his study of the biological functions of the Fas death pathway.

Fas pathway plays a critical role in the pathogenesis of T1D in animal models and its blockade with neutralizing mAbs prevents disease in animals. Currently, Dr. Hamad is working along with Dr. Thomas Donner, Director of Diabetes at Johns Hopkins Hospital to translate these findings to human diseases. 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.

Dr. Hamad and colleagues have also shown that intact Fas pathway is necessary for compartmentalizing a subset of T cells called double negative (DN) alpha/beta T cells in the gut epithelium. In addition, he and his collaborator, Dr. H. Rabb, Director of Medical Kidney transplantation at Hopkins, have shown that the kidney is a major residence site of DN T cells where they actively proliferate in the steady state and play a critical role 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 for 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 findings ways to translate these findings into therapeutic for obesity.

Dr. Hamad is 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.

 

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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

Hamad AR, Arcara K, Uddin S, Donner T. 2012. The potential of Fas ligand (apoptosis-inducing molecule) as an unconventional therapeutic target in type 1 diabetes, Frontiers in immunology, 3:196

Gutfreund, R., and A. R. Hamad. 2011. Immunotherapy for Type 1 Diabetes: Necessity, Challenges and Unconventional Opportunities. Book chapter in: Type 1 Diabetes - Pathogenesis, Genetics and Immunotherapy. D. Wager, ed. INTECH, Janeza Trdine 9. 409-424.

Xiao, X., Mohamood, A.S., Uddin, S., Gutfreund, R., Nakata, S., Marshall, A., Kimura, H., Caturegli, P., Womer, K.L., Huang, Y., J. Schneck, Hideo Yagita and Abdel Rahim A. Hamad. 2011. Inhibition of Fas ligand in NOD mice unmasks a protective role for IL-10 against insulitis development. Am J Pathol. 179:725. PMID 21718680.

Ko, G.J., Jang, H.R., Huang, Y., Womer, K.L., Liu, M., Higbee, E., Xiao, Z., Yagita, H., Racusen, L., Hamad, A.R.A., and Rabb, H. 2011. Blocking fas ligand on leukocytes attenuates kidney ischemia-reperfusion injury. J Am Soc Nephrol 22, 732-742. PMID: 21436290

Abdel Rahim Hamad. 2010. Analysis of gene profile, steady state proliferation and apoptosis of double negative T cells in the periphery and gut epithelium provides new insights into the biological functions of the Fas pathway. Immunol. Res. 47:134-42. PMID 20066510

Mohamood AS, Bargatze D, Xiao Z, Jie C, Yagita H, Ruben D, Watson J, Chakravarti S, Schneck JP, Hamad ARA. 2008. Fas-mediated apoptosis regulates the composition of peripheral alpha/beta T cell repertoire by constitutively purging out double negative T cells. PLoS ONE 3:e3465. PMID 18941614

Hamad ARA, Marrack P, Kappler J. Transcytosis of staphylococcal superantigen toxins. J Exp Med 1997; 185:1447-54. PMID: 9126925

Hamad ARA, Herman A, Marrack P, Kappler J. Monoclonal antibodies defining functional sites on the toxin superantigen staphylococcal enterotoxin B. J Exp Med 1994; 180:615-21. PMID: 7519243

Hamad ARA, Oherrin S, Sriskrishnan A, Bieler J, Schneck J, Pardoll D. Potent T cell activation with dimeric MHC Class II- peptide complex: The role of CD4 molecule. J Exp Med 1998; 188:1633-40. PMID: 9802975

Hamad ARA, Srikrishnan A, Breueren C, June C, Pardoll D, Schneck J. Lack of coreceptor allows survival of chronically stimulated CD4-CD8-B220+ T cells: Implications for autoimmunity. J Exp Med 2001; 193:1113-21. PMID: 11369783

Xiao X, Mohamood AS, Uddin S, Gutfreund R, Nakata S. Marshall A, Kimura H, Caturegli P, Womer KL., Huang Y, Schneck J, Yagita H, Hamad AR. Inhibition of Fas ligand in NOD mice unmasks a protective role for IL-10 against insulitis development. Am J Pathol 2011;179:725. PMID: 21718680

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

Dai H, Rahman A, Saxena A, Jaiswal AK, Mohamood A, Ramirez L, Noel S, Rabb H, Jie C, Hamad AR. Syndecan-1 identifies and controls the frequency of IL-17-producing naïve natural killer T (NKT17) cells in mice. Eur J Immunol. 45:3045-51. 2015. PMID: 26300525

Martina MN, Noel S, Saxena A, Bandapalle S, Majithia R, Jie C, Arend LJ, Allaf ME, Rabb H, Hamad AR. Double-Negative αβ T Cells Are Early Responders to AKI and Are Found in Human Kidney. J Am Soc Nephrol. 2015 Aug 27. PMID: 26315532

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