Colleagues: Recently Tenured

Meet your recently tenured colleagues: Behdad Afzali (NIDDK), Farran Briggs (NEI), Peng Jiang (NCI-CCR), and Melissa Wilson (NHGRI).

Behdad (Ben) Afzali, M.D., Ph.D.

Senior Investigator, Immunoregulation Section, Kidney Diseases Branch (NIDDK)

Education: Guy’s and St Thomas’, University of London, London (B.S. in immunology); Guy’s, King’s, and St Thomas’, University of London (M.D.); King’s College, London, University of London (Ph.D. in immunology); Royal College of Physicians (UK) (F.R.C.P.)

Training: Postgraduate Diploma in Medical Education (PGDip), Institute of Education, London; Residency Oxford Medical Rotation, Oxford, England (2001–2003); Nephrology Fellowship, South Thames, London (2004–2012)

Before coming to NIH: Wellcome Trust Intermediate Clinical Research fellow, King’s College London, London, and John O’Shea’s lab at NIAMS (2012–2017)

Came to NIH: In 2018 as a Stadtman tenure-track investigator and consultant nephrologist, NIDDK

Outside interests: Reading; photography; cycling

Website: https://irp.nih.gov/pi/behdad-ben-afzali

Research interests: Our research seeks to understand the molecular mechanisms that drive tissue inflammation, a process that underlies a substantial proportion of deaths worldwide from chronic diseases. Despite its enormous impact, tissue inflammation remains poorly understood, and current treatments rely on drugs that are nonspecific and toxic. Our mission is to uncover how microenvironmental cues initiate and sustain tissue inflammation, how networks of transcription factors within immune cells integrate these signals to determine their fate and function, and how tissue inflammation is either resolved, restoring healthy tissue, or progresses to maladaptive scarring. A particular emphasis is placed on understanding how these transcriptional networks operate not only in immune cells but also in tissue-resident cells. Examples of our work include the identification of transcription factor networks that drive pathogenic versus regulatory states in both immune and non-immune cells during tissue inflammation, including those leading to local production of complement components and receptor signaling (PMID: 30397350; PMID: 32187519; PMID: 33827897; PMID: 34764490).

Future research: The long-term aim is to identify actionable immunoregulatory nodes for therapeutic exploitation to shift the balance between destructive inflammation and protective regulation, or between tissue scarring and healing. Ultimately, our work seeks to move toward more precise therapies that resolve inflammation more effectively, with fewer side effects, and that improve the quality of life for patients living with chronic inflammatory diseases.

[Compiled by John Carlo Combista, NIMH]

Farran Briggs, PH.D.

Senior Investigator, Thalamocortical Visual Processing Section (NEI)

Education: Dartmouth College, Hanover, New Hampshire (B.S. in biology); University of California at San Diego, San Diego (Ph.D. in biology)

Training: Postdoctoral fellow, University of California at Davis, Davis, California (2003-2010)

Before coming to NIH: Associate professor of Neuroscience, Brain & Cognitive Sciences, University of Rochester, Rochester, New York; Assistant professor of Physiology & Neurobiology, Geisel School of Medicine, Dartmouth College, Hanover, New Hampshire (2011-2017)

Came to NIH: In 2024 as a senior investigator, NEI

Outside interests: I am an outdoorsy person who loves to run and cycle. I just returned from a pretty epic trip around the French Alps, riding the same mountains as the Tour de France, and managed to watch some of the Tour de France. It was a once in a lifetime experience.

Website: https://irp.nih.gov/pi/farran-briggs

Research interests: I am probably best known for my contributions to our understanding of what feedback from the cortex to the thalamus does functionally in the sensory system, specifically in vision. Much progress has been made in restoring retinal tissue and improving visual functions via retinal prosthetics. However, retinal disease does not just affect the eye, it also causes significant functional remodeling in the brain. My lab’s recent paper demonstrates that loss of retinal cells reduces functionality of neurons in the brain center to which they project that are specialized for acuity, while neurons specialized for motion perception in the same center are relatively spared (PMID: 40300832). These results suggest that vision restoration after retinal damage should include therapies that target neuronal pathways specialized for acuity. Our work has been highlighted in NEI Research News. An offshoot of this paper is that some of the downstream effects we see after retinal damage have similar electrophysiological profiles as in patients with schizophrenia. And so, I’m really excited about our work having broad translational implications.

Future research: One of the reasons that I decided to come to NEI is because of my bigger picture: The dream experiments, that in academia, wouldn’t be feasible. NEI is the kind of place where I can start working on my various interests. I would really like to be able to causally manipulate feedback circuits between cortex and thalamus among different cortical areas using sophisticated molecular (viral) tools.

[Compiled by Anneliese Norris, NCI-CCR]

Peng Jiang, Ph.D.

Senior Investigator, Cancer Data Science Laboratory (NCI-CCR)

Education: Tsinghua University, Beijing, China (B.E. in computer science); Princeton University, Princeton, New Jersey (Ph.D.)

Training: Postdoctoral fellow, Dana Farber Cancer Institute, Harvard University, Boston (2013-2019, Xiaole Shirley Liu Laboratory)

Came to NIH: In 2019 as a Stadtman tenure-track investigator, NCI

Website: https://irp.nih.gov/pi/peng-jiang

Research interests: My research focuses on developing data-integration and artificial-intelligence frameworks (PMID: 36064595) to study intercellular signaling mediated by secreted and extracellular proteins in antitumor immunity. Data-driven analyses estimate that about 2,000 human genes encode secreted proteins. Yet, our literature mining revealed that 61% of these genes lack known roles in cancer. To address this gap, we develop computational methods and apply diverse immunological models to dissect cytokine networks [(PMID: 34594031; PMID: 35501486); secreted proteins (PMID: 40730154); ligand–receptor interactions (PMID: 36732531)] in cancer. Ultimately, our goal is to uncover new mechanisms of immune regulation and identify therapeutic opportunities that harness intercellular communication against tumors.

Future research: In the next stage, we aim to identify new secreted proteins regulating antitumor immune response by combining data integration, spatial transcriptomics, and artificial-intelligence frameworks. Also, we want to establish long-term collaborations with clinical investigators for translational works.

[Compiled by John Carlo Combista, NIMH]

Melissa Wilson, Ph.D.

Senior Investigator, Center for Genomics and Data Science Research (NHGRI)

Education: Creighton University, Omaha, Nebraska (B.S. in Mathematics); Pennsylvania State University, University Park, Pennsylvania (Ph.D. in bioinformatics and genomics)

Training: Miller Postdoctoral Fellowship, Berkeley University, Berkeley, California (statistics and integrative biology) (2011-2014)

Before coming to NIH: Tenured professor, School of Life Sciences at Arizona State University, Tempe, Arizona (2014-2024)

Came to NIH: December 2024 as a senior investigator, NHGRI

Outside interests: Parenting; science communication; exploring nature; cooking

Website: https://www.genome.gov/about-nhgri/Division-of-Intramural-Research/Cent…

Research interests: I am a geneticist and computational biologist broadly interested in sex differences in health and disease. Specifically, my lab collaborates with clinicians, physiologists, and computer scientists to understand the cause and consequences of sex differences in human and nonhuman animals. We take multiple approaches to understanding sex differences, broadly separated into methodology and implementation.

“First we develop novel methodology for incorporating the sex chromosomes into genomics analyses. Most genetics methodology was developed for the autosomes (non-sex chromosomes), and often the X and Y break basic assumptions of these approaches. My lab has developed approaches to improve the detection of DNA variants (PMID: 31289836) and improve the quantification of RNA abundance (PMID: 32693839) on the sex chromosomes. We’ve further provided best practices for testing genetic models of sex differences in human cohorts (PMID: 37172561).

Second, we are active in assessing the effects of sex as a biological variable on human health and disease. We have shown that sex differences in gene expression early in life persist across adult tissues later in life (PMID: 36550527). We have further identified sex differences in gene expression and mutational processes in liver cancer, suggesting distinct etiologies (PMID: 31615477). Further, as part of a collaborative project on Alzheimer’s disease, we identified, for the first time, a sex-linked transcription factor pair (ZFX/ZFY) associated with more pronounced neuronal loss in females (PMID: 40670382), underscoring the importance of accurately incorporating the X and Y chromosomes into human genetics analyses.

Future research:

• Studying molecular sex differences during pregnancy and placentation that affect fetal and maternal health
• Measuring the functional consequences of the loss of X and Y in cancer
• Improving methodology for molecular identification and analysis of the X and Y chromosomes
• Studying the effects of sex chromosome dosage and X-inactivation on human health

[Compiled by Taylor Farley, VRC]