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Nicholas M. Stamatos, MD, PhD

Academic Title:

Associate Professor

Primary Appointment:


Additional Title:

Member, Institutional Review Board


UMBI Room N558

Phone (Primary):

(410) 706-2645


(410) 706-1992

Education and Training

1977    B.A.     Boston University, Boston, MA
1987    Ph.D.   University of Rochester School of Medicine, Rochester, NY

1991    M.D.    George Washington University School of Medicine, Washington, DC

Internship/Residency (Internal Medicine)

1991-1994       Walter Reed Army Medical Center, Washington, DC


1997-1998       Infectious Diseases, University of Maryland School of Medicine, Baltimore, MD


Dr. Stamatos’ academic career combines the challenges and rewards of practicing clinical medicine and conducting basic research.  He attends on the HIV/Medicine inpatient service and on the Infectious Diseases Cancer Center/Bone Marrow Transplant and Medical Intensive Care Unit consult services, as well as at an outpatient Infectious Diseases clinic.  He plays an integral role in training Infectious Disease fellows, postdoctoral research fellows, medical housestaff and students in both the clinic and the laboratory.  With a special interest in virology and glycoimmunology, he also conducts research that is focused on understanding how modulation of the carbohydrate content of cell surface glycoproteins and glycolipids influences the functional capacity of peripheral blood mononuclear cells, including their interaction with HIV-1.  His laboratory has shown that desialylation of glycoconjugates on the surface of purified human monocytes activates cells, stimulates production of cytokines (e.g. IL-12p40, TNFa, and IL-6), and enhances the responsiveness of monocytes to lipopolysaccharide (LPS).  His work suggests that inhibition of endogenous sialidases may be a therapeutic target during LPS-mediated infections.  His work also pioneered the growing appreciation that Neu1 sialidase, previously deemed to be strictly a lysosomal protein, is present and active on the cell surface.  His laboratory was first to show the importance of polysialic acid (polySia) in the immune system by demonstrating that neuropilin-2 (NRP-2) is expressed on the surface of human dendritic cells (DC) and is polysialylated.  His laboratory’s discovery of polysialylated NRP-2 on DC has engendered numerous studies from other laboratories that demonstrate a direct role of polySia in DC migration and has generated great interest in identifying additional polysialylated cells in the immune system. Although much is known about the glycosylation of HIV-1 envelop proteins, relatively little is known about how glycosylation of proteins on the surface of permissive lymphocytes affects infection.  He previously demonstrated that removal of sialic acid from the surface of peripheral blood mononuclear cells using an exogenous bacterial neuraminidase promoted infection with HIV-1. In contrast to work on monomeric sialic acid, he has also found that removal of polySia from a specific protein on the surface of lymphocytes or in the extracellular milieu markedly inhibits infection.  The results from his studies are expected to identify a novel target for treatment of HIV infection and provide a blueprint for down-regulating the expression of polySia or modified protein(s) in activated lymphocytes, as well as in other cells susceptible to infection with HIV-1.  The overarching goal of research in his laboratory is to demonstrate that sialic acid, sialidases and sialyltransferases are potential targets for therapeutic agents during infectious and inflammatory conditions.

Research/Clinical Keywords

Clinical infectious diseases, immunocompromised hosts, glycoimmunology, neuropilins, semaphorins

Highlighted Publications

Curreli, S., Wong, B.S., Latinovic, O., Konstantopoulos, K. and Stamatos, N.M.  2016.  Class 3 semaphorins induce F-actin reorganization in human dendritic cells: role in cell migration  J. Leukoc. Biol. Dec;100(6):1323-1334.  PMID: 27406993


Stamatos, N.M., Zhang, L., Jokilammi, A., Finne, J., Chen, W.H., El-Maarouf, A., Cross, A.S. and Hankey, K.G.  2014.  Changes in polysialic acid expression on myeloid cells during differentiation and recruitment to sites of inflammation: Role in phagocytosis.  Glycobiology 24(9):864-79.  PMID: 24865221


Stamatos, N.M., Carubelli, I., van de Vlekkert, D., Bonten, E.J., Papini, N., Feng, C., Venerando, B., d'Azzo, A., Cross, A. S., Wang, L. X. and P. J. Gomatos.  2010. LPS-induced cytokine production in human dendritic cells is regulated by sialidase activity.  J. Leukoc. Biol. 88(6):1227-39.   PMID: 20826611


Curreli, S., Arany, Z., Gerardy-Schahn, R., Mann, D. and Stamatos, N.M.  2007. Polysialylated neuropilin-2 is expressed on the surface of human dendritic cells and modulates dendritic cell-T lymphocyte interactions.  J. Biol. Chem. 282:30346-56.    PMID: 17699524


Stamatos, N.M., Gomatos, P. J., Cox, J., Fowler, A., Dow, N., Wohlhieter, J.A. and Cross, A.S.  1997.  Desialylation of peripheral blood mononuclear cells promotes growth of HIV-1.  Virology 228:123-131.    PMID: 9123818