Abdel R. Hamad

Abdel R. Hamad, DVM, Ph.D.
DVM – University of Khartoum, Sudan
Ph.D – University of Colorado Health Sciences Center

Associate Professor, Department of Pathology
The Johns Hopkins University School of Medicine
The Richard Starr Ross Research Bldg.
720 Rutland Ave., Room 659
Baltimore, Maryland 21205

Phone: (410) 614-3021
E-mail: ahamad@jhmi.edu

   

Research

Keywords:  T cell development; tolerance; Fas pathway; immunoregulation; type 1 diabetes; lymphoproliferation.

Unlocking the biological mysteries of the Fas pathway in regulating T cell homeostasis and organ specific T cell tolerance.

Although the Fas death pathway is important for elimination of autoreactive T cells, loss-of-function mutations of Fas (lpr) or its ligand (gld) prevent rather than enhances organ specific autoimmune disease such as type 1 diabetes and multiple sclerosis in animal models. Another mystery associated with lpr and gld phenomena is the lymphoproliferative accumulation of CD4-CD8-double negative (DN) abT cells that express B220 molecules but whose function is unclear. Similar B220+DN abT cell lymphoproliferation occurs in humans with impaired Fas pathway. Revealing the nature of DN T cells that cause lymphoproliferation in mutant mice and understanding how impairment of the Fas pathway confers organ-specific-tolerance are the two major areas research in our lab. Our recent data indicate that these so called abnormal DN T cells are likely an independent cell subset that develop in the thymus and is confined to the gut epithelium in normal animal due to their deletion by Fas-mediated apoptosis in the periphery. Consequently, impairment of the Fas pathway results in peripheral accumulation of these DN T cells in the periphery. On the other hand, indicate that a tissue specific regulatory B cells are actively deleted by Fas-mediated apoptosis and removed from pancreas of autoimmune prone NOD mice. When present in the pancreas as a result of FasL blockade these B cell subset prevent diabetogenic T cells from invading and destroying pancreatic islets by an IL-10 dependent mechanism. How these IL-10 producing B cells are recruited into the pancreas and why eliminated by Fas-mediated apoptosis in the steady state is actively investigated in the lab.

Profile: Publications and Interests

https://jhu.pure.elsevier.com/en/persons/abdel-r-hamad