For a better experience, click the Compatibility Mode icon above to turn off Compatibility Mode, which is only for viewing older websites.

Potential of the Flavonoid Apigenin in Regulating Immune Cell Functions

Thursday, November 30, 2017

10:00 AM-12:00 PM

BIOMED PhD Research Proposal

Potential of the Flavonoid Apigenin in Regulating Immune Cell Functions During Neuroinflammation in a RelB-dependent Manner

Rashida Ginwala, PhD Candidate, School of Biomedical Engineering, Science and Health Systems

Pooja Jain, PhD, Professor, Department of Microbiology and Immunology, College of Medicine, Drexel University

Adrian Shieh, PhD, Associate Professor, School of Biomedical Engineering, Science and Health Systems, Drexel University

Apigenin, a natural flavonoid found in several plants, is known to have anti-oxidant and anti-inflammatory properties; however, its effect on dendritic cell (DC) function in maintaining an immune balance in an immunospecialized location like the central nervous system (CNS) is not well-studied.

To establish the potential utility of Apigenin as a therapeutic agent against neuroinflammatory diseases, we tested and found that Apigenin treatment ameliorated severity of disease progression and relapse after onset of experimental autoimmune encephalomyelitis (EAE) in C57BL/6 and SJL mouse models of multiple sclerosis. Apigenin treated EAE mice showed decreased expression of α4 integrin (adhesion) and CLEC12A (antigen uptake) on splenic DCs. An increased retention of DCs and other myeloid cells in the periphery correlated with decreased immune cell infiltration and reduced demyelination in the CNS.

Additionally, both ex vivo antigen-dependent and antigen-independent immune cell responses were modulated by Apigenin with distinct polarization towards a regulatory phenotype. Mechanistically, Apigenin treatment reduced cytoplasmic RelB expression in presence of LPS in human peripheral blood DCs, which is central to DC maturation, its antigen presentation capabilities and DC-mediated T cell activation. TNF-α and IL-23, downstream targets of RelB were also reduced upon Apigenin treatment in these cells. RelB also plays a role in mitochondrial bioenergetics during inflammation, which explains the metabolic shift away from glycolysis observed upon Apigenin treatment in the inflamed DCs. These results indicate a protective role of Apigenin against neurodegenerative DC-regulated effects through a probable RelB mediated pathway thus implicating a potential therapy for neuroinflammatory disease.

Contact Information

Ken Barbee

Remind me about this event. Notify me if this event changes. Add this event to my personal calendar.


Bossone Research Center, Room 709, located at 32nd and Market Streets.


  • Undergraduate Students
  • Graduate Students
  • Faculty
  • Staff