Colleagues: Recently Tenured

ANDRE BALLESTEROS-TATO, PH.D., NIAID

Senior Investigator, Chief, Adaptive Immunity and Immunoregulation Section, NIAID

Education: University of Vigo, Vigo, Spain (B.S. in biology); Autónoma University, Madrid (Ph.D. in molecular biology)

Training: Postdoctoral research fellow, Trudeau Institute, Saranac Lake, New York (2008); University of Rochester, Rochester, New York (2008–2012); University of Alabama at Birmingham, Birmingham, Alabama (2012)

Before coming to NIH: Professor, Department of Medicine, University of Alabama at Birmingham

Came to NIH: In 2024 as senior investigator, NIAID

Outside interests: Reading; cooking; exercise; spending time with family

Website: https://www.niaid.nih.gov/research/andre-ballesteros-tato-phd

Research interests: My primary research interest is to define the cellular and molecular mechanisms that balance protective and pathogenic adaptive immune responses to allergens. The ultimate aim of my work is to develop innovative immunotherapies for treating and preventing food and respiratory allergies without causing significant immunosuppression. Leveraging advanced cellular and molecular techniques, my group has deep expertise in studying adaptive immune responses to respiratory pathogens and allergens (PMID: 37699392; PMID: 34516781; PMID: 31519812; PMID: 28892471).

My research focuses on three main areas:

1. Characterizing the mechanisms that regulate adaptive immune responses—particularly memory T and B cells and T follicular helper cells—in the context of food and respiratory allergies.
2. Investigating the interplay between infections and allergies to understand how infections may contribute to allergy development and how existing allergies influence immune responses to pathogens and vaccines.
3. Developing novel immunotherapies that achieve a balance between protection and controlled immunosuppression for food and respiratory allergens.

YARIMAR CARRASQUILLO, PH.D., NCCIH, NIDA

Senior Investigator, Pain Neurocircuitry and Cellular Plasticity Lab, NCCIH, NIDA

Education: University of Puerto Rico, Rio Piedras, Puerto Rico (B.S. in biology); Baylor College of Medicine, Houston (Ph.D. in neuroscience)

Training: Postdoctoral research scholar, Washington University, St. Louis (2005–2011)

Before coming to NIH: Staff scientist, Washington University, St. Louis (2011–2013)

Came to NIH: In 2014 as a principal investigator, NCCIH

Outside interests: Cycling; hiking; anything outdoorsy

Website: https://www.nccih.nih.gov/research/intramural/intramural-labs/pain-neurocircuitry-and-cellular-plasticity-lab

Research interests: I am a neuroscientist specializing in studying pain. My lab is interested in identifying brain mechanisms underlying bidirectional modulation of pain and in determining whether these processes are sex dependent. We use multidisciplinary approaches that include cellular physiology, molecular genetics, neuroanatomy, and behavioral rodent assays to tackle questions at molecular, cellular, and circuit levels that we then causally link to pain-related behaviors.

We have focused on the central amygdala (CeA), a forebrain limbic structure well positioned to link noxious stimuli to defense and affective responses. Our studies uncovered a dual function of the CeA in pain processing, showing that this brain region bidirectionally modulates pain and that the directionality of pain modulation is encoded by cell-type-specific changes in neuronal activity (PMID: 31597095). At the cellular level, we have shown that genetically distinct CeA neurons are also morphologically and electrophysiologically distinct (PMID: 33188006; PMID: 34101729) and that neurons in the parabrachial nucleus (a brain region that relays nociceptive inputs to the CeA) undergo divergent changes in excitability after an injury (PMID: 38331576).

At the circuit level, we identified and functionally characterized CeA efferent and afferent projections that modulate pain-related behaviors (PMID: 36269044;PMID: 36473754; PMID: 37542159). Our studies have further shown important sex differences in brain mechanisms of pain modulation (PMID: 35559931). In a recent study, we further showed that neuroplastic processes in amygdala cells and circuits contributing to increased pain after an injury are time-dependent, demonstrating that chronic pain is mechanistically distinct from acute pain (PMID: 39178115).

Future directions: When studying pain, it is important to recognize that pain is not experienced in isolation from other stimuli or physiological states and needs. Behavioral and physiological responses to internal and external stimuli (e.g., injury, hunger, threat, reward, mild and chronic stress) are known to reciprocally influence each other. Our ongoing efforts are focused on studying the CeA neurons and inputs and outputs involved in situations presenting competing pressures in pain states. Our ultimate goal is to build a CeA circuit map with synaptic and cellular components describing cell-type and pathway-specific functions of distinct pain-related behaviors.

[COMPILED BY SEPPIDEH SAMI, CC]

BEATRIZ LEÓN, PH.D., NIAID

Senior Investigator, Laboratory of Allergic Diseases, Innate Cells and Th2 Immunity Section, NIAID

Education: Complutense University, Madrid (B.S. in biology); Autónoma University, Madrid (Ph.D. in molecular biosciences)

Training: Postdoctoral fellow, Autónoma University (2007–2008); postdoctoral fellow, Trudeau Institute, Saranac Lake, New York (2008); postdoctoral fellow, University of Rochester, Rochester, New York (2008–2012); postdoctoral fellow, University of Alabama at Birmingham, Birmingham, Alabama (2012)

Before coming to NIH: Tenured associate professor, University of Alabama at Birmingham

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

Outside interests: Outdoor adventures; family movie nights; reading; indoor plant growing

Website: https://www.niaid.nih.gov/research/beatriz-leon-phd

Research interests: I am an immunologist dedicated to uncovering the immunological mechanisms behind allergies. I recently joined the Laboratory of Allergic Diseases, where I lead the Innate Cells and Th2 Immunity Section. Our section integrates mouse models, immunological techniques, and next-generation molecular tools to investigate how common airborne allergens trigger and sustain allergic diseases. Additionally, we explore how genetic factors, environmental exposures, microbiota, diet, and other influences contribute to these processes.

One of our key interests is understanding why and how inhalant allergens are perceived as pathogenic by the immune system and how they initiate harmful immune responses—leading to allergy (PMID: 37810200)—and sustain chronic inflammation over the long term (PMID: 26825674).

Another focus is identifying genetic and environmental risk factors that predispose individuals to allergies or, conversely, provide protection (PMID: 37100645; PMID: 36704753). Our lab has identified genetic risk factors for airway allergies (PMID: 37046042; PMID: 34965421) and uncovered mechanisms driving susceptibility to allergic diseases during critical periods such as infancy (PMID: 30635238). We will continue to explore environmental influences, including diet, gut microbiota, and metabolism, to understand how these factors affect allergy risk during vulnerable windows such as infancy, pregnancy, and the impact of genetic defects.

Future directions: In our future research, we hope to identify potential intervention targets for preventing or treating allergic diseases.

CHUAN WU, M.D., PH.D., NCI

Senior Investigator, Experimental Immunology Branch, Center for Cancer Research, NCI

Education: Shanghai Jiao Tong University School of Medicine, Shanghai (M.D. in clinical medicine); Münster University, Münster, Germany (Ph.D. in immunology)

Training: Postdoctoral fellow, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston (2010–2015)

Before coming to NIH: Assistant professor, Brigham and Women’s Hospital, Harvard Medical School

Came to NIH: In 2017 as an Earl Stadtman Investigator, NCI

Outside interests: Painting; running; music

Website: https://irp.nih.gov/pi/chuan-wu

Research interests: Barrier surfaces are an innate immune mechanism that enforce host-microbe homeostasis by controlling physical access of microbes and their products to the body. The gastrointestinal tract mucosa represents the largest interface in apposition with the commensal microbiome. My lab is interested in understanding intercellular regulation on intestinal barrier integrity. We have contributed impactful discoveries concerning intercellular cross-talk in mediating gut homeostasis by regulating epithelial barrier integrity, host-commensal symbiosis, neuroendocrine homeostasis, and immune balance, which are correlated to inflammatory bowel disease and colon cancer.

My lab identified that intestinal epithelial cells play a critical role in establishing commensalism and maintain intestinal barrier integrity (PMID: 34287641). Further, our work suggests that goblet-cell-mediated protein sialyation is crucial for intestinal mucus integrity and host-microbial homeostasis (PMID: 35303419). More recently, my lab established the role of the gut-liver axis in intestinal stem-cell fitness (PMID: 38280375). We also made discoveries in T-cell responses for mucosal tolerance and barrier integrity, which led to several impactful publications (PMID: 29346764; PMID: 37040761; PMID: 37436991; PMID: 37429951). Additionally, we made significant contributions towards understanding immune-neuron cross-talk for intestinal neuroendocrinal homeostasis, particularly in controlling serotonin release for local and systemic physiology (PMID: 33220232; PMID: 34871362; PMID: 37354904).

Future directions: My lab currently is pursuing mechanistic studies for the intercellular regulation of mucosal barrier function. Our studies of cellular and molecular machineries of cell-cell interactions for regulating intestinal barrier function will have broad implications across the fields of immunology, physiology, and neuroendocrinology.