Ben Afzali studied medicine at the United Medical and Dental Schools of Guy’s and St Thomas’ hospitals, in the United Kingdom, from 1994-2000, qualifying as Valedictorian of his year. Following his primary medical degree, he undertook residency training in internal medicine on the Oxford medical rotation from 2001-2003, during which time he successfully completed the examination requirements for membership of the royal college of physicians. He then commenced fellowship training in renal medicine on the South Thames London rotation, most of which was spent at Guy’s hospital, and was subsequently appointed as an honorary consultant nephrologist at Guy’s. Ben’s research career began during his primary medical studies, which intercalated a Bachelor of Science in Immunology, awarded with first class honors, focused on the role played by adhesion molecules in autoimmunity. He studied for a PhD in immunoregulation with a focus on regulatory T cell (Treg) biology under the supervision of Professors Sir Robert Lechler and Giovanna Lombardi at King’s College London. He was awarded the degree of Philosophical Doctorate in 2009 from the University of London and went on to be appointed as a clinical lecturer. He was the recipient of a Wellcome Trust intermediate Clinical Fellowship to investigate the transcriptional mechanisms by which regulatory T cells produce soluble factors and their impact for cell therapy. As part of this fellowship he was a guest researcher in the laboratory of Dr John O’Shea at the National Institute of Arthritis and Musculoskeletal and Skin Diseases from 2014 where he examined key transcription factors involved in Treg biology, notably BACH2 and STAT5. He is currently an Earl Stadtman investigator in NIDDK and studies renal immunoregulation, notably how environmental signals in tissues are integrated via networks of transcription factors to direct the basic mechanisms of autoimmunity, subsequent tissue injury and wound healing.
Daniel graduated from the University of North Florida with a B.S. in Biology in 2010 with a focus in Evolutionary Genetics before beginning graduate work at Florida Atlantic University with Marc Kantorow. During his graduate work, Daniel used modern molecular biology and bioinformatics tools to elucidate those processes that drive developmental and protective mechanisms of eye tissue. This work culminated with the discovery that specialized eye tissue retains immunological features in the absence of classical immune cells to protect against environmental damage. Leveraging this work, Daniel began his time at NIH in the Nuclear Lymphocyte Laboratory in NIAMS where he gained training in multi-dimensional transcriptomics, epi-regulation and CRISPR/Cas9 before beginning in the Immunoregulation Laboratory at NIDDK. Daniel integrates state of the art sequencing and genome editing tools to dissect fundamental molecular mechanisms driving cell-state and cellular identity. By analysis of cell-specific epi-regulomes and downstream expressed molecules, Daniel’s work seeks to identify the underlying biological requirements altered in various modes of autoimmunity and complex disease. Under this umbrella, Daniel’s research aims to find those fundamental triggers so that they can be modulated and harnessed for the development of new therapeutics.
Nardos graduated from the University of Virginia with a Bachelor of Science degree in Chemistry, with specialization in Biochemistry, in May 2018. Concurrently with her studies she worked as a research assistant in the Center for Immunity, Inflammation and Regenerative Medicine and interned on the summer medical and dental education program (SMDEP) of the university.
Tilo Freiwald obtained an MD and doctorate from the University Hospital Hamburg Eppendorf. He is an internal medicine specialist at the University Hospital of Frankfurt with a clinical focus on kidney transplantation. He is a co-founder and developer of a leading medical e-learning platform. Tilo’s main interest is the role played by complement-triggered signals in kidney diseases and computational modelling of disease progression and resolution.
Didier Portilla is Professor of Medicine in the Division of Medicine at the University of Virginia and a research collaborator of the Immunoregulation section. His research interests include acute and chronic kidney injury and transcriptional control exerted by mediators of kidney injury on renal scarring.
The overall goal of his research is to understand the cellular and molecular mechanisms that contribute to proximal tubule cell death during Acute Kidney Injury (AKI). His laboratory has elucidated the role that increased lipotoxicity plays in the pathogenesis of proximal tubule cell death and tubulo-interstitial fibrosis, using both in vivo and in vitro models of ischemia-reperfusion and unilateral ureteral obstruction. His studies support the notion that PPARalpha, a nuclear receptor transcription factor expressed in the proximal tubule and also in interstitial pericytes/fibroblasts, serves as an important metabolic sensor for lipid homeostasis. When stimulated by either a ligand or by using transgenic mice, his research finds that PPARalpha mediates cytoprotection by reducing inflammation and renal fibrosis. Didier’s work has been funded by an NIH RO1 and by VA Merit Award, and examines the role and mechanisms by which PPARa signaling increases mitochondrial fatty acid oxidation, prevents renal fibrosis and pericyte to myofibroblast transformation. He has served as Program Director of the NIDDK T32 Training program in the Pathophysiology of Renal Disease at the University of Arkansas in Little Rock. During that time (2009-2014), he has mentored several postdoctoral fellows in his laboratory, some of them promoted to junior faculty positions. Since his arrival to University of Virginia in July 2014, he served as Co-Associate Director of theT32 Training Program at the Division of Nephrology and has mentored junior faculty members of his Division. He has developed C1r null mice to study the function of C1 complex proteases C1r and C1s and has also obtained C5aR1 GFP reporter mice where he has shown that pericytes and CD45 F4/80 cells express higher levels of this receptor in animal models of fibrosis. He has used these mice to cross them with FoxD1 Cre and LysM Cre to examine the role of tissue specific deletion of C5aR1 during kidney fibrosis.
Huzaifah graduated from Virginia Commonwealth University with a Bachelor of Science degree in May 2018 with experience in biomaterial research as an undergraduate. Huzaifah is inspired by the potential of translational immunological research for patient care. In his free time, you will find him hiking.