The Unutmaz Lab investigates the biology of the human immune system.
Our research primarily focuses on decoding the differentiation, activation and regulation of human T cells for optimal immune responses to infectious diseases and their perturbations during chronic diseases or aging. We have contributed to the understanding of how T cell subsets are disrupted during human diseases, especially during HIV infection. Our lab has made several seminal discoveries about the diversity and mechanisms of immune suppression mediated by regulatory T cells and effector functions of human Th17 cell subsets.
Derya Unutmaz and Julia Oh are helping to remove the obstacles for diagnosing Myalgic Encephalomyelitis/Chronic Fatigue...
Immune phenotyping of ME/CFS, MIS-C and Long COVID
Grant to JAX Professor Derya Unutmaz, M.D., part of multi-institutional research effort to understand and treat Myalgic...
A collaborative JAX research center led by Derya Unutmaz is diving deep into the biology of ME/CFS patients to find a root...
JAX professor Derya Unutmaz, a renowned expert in HIV, launches a bold initiative to examine how immune system aging...
We interviewed Courtney Gunter, program manager for the JAX ME/CFS research center, to get her perspective on this mysterious disease and...
Derya Unutmaz, M.D., will receive five years of funding totaling $3,281,515 from the National Institute of Allergy and...
Researches the mechanisms of human T cell differentiation, activation and regulation in the contexts of normal immune...
Chronic fatigue syndrome is frustrating on all fronts. It's difficult to diagnose, difficult to treat and a pain to live...
What is a mouse model? Find out in this Minute to Understanding from the Jackson Laboratory!
JAX Professor Derya Unutmaz, M.D., speaks about his work searching for new effective treatments for chronic illnesses like...
More than 140 current research grants from the National Institutes of Health (NIH) are for multi-institutional projects that are either led...
Inducible/constitutive CRISPR activation, deletion and knock-in systems on transformed and primary human T cells.