Choi (Jaehyuk) Lab

Pioneering therapies for immune-related diseases.

About Us

The goal of the Choi Lab is to develop novel immunotherapies. To accomplish this, we first utilize high-dimensional approaches on human disease samples. This approach identifies targetable disease-promoting molecular defects in immune cells. Then, we utiize engineering approaches to reverse molecular changes.

Meet the PI

Jaehyuk Choi, M.D., Ph.D.

Jaehyuk Choi, M.D., Ph.D.

Dr. Choi the inaugural Director of the new Center for Cellular Therapies and Cancer Immunology in the Harold C. Simmons Comprehensive Cancer Center. He also serves as Vice Chair for Translational Research and Innovation in the Department of Dermatology and holds the Scheryle Simmons Patigian Distinguished Chair in Cancer Immunobiology. After completing undergraduate studies in biochemistry at Harvard University, Dr. Choi earned his medical degree and Ph.D. in immunobiology from Yale University School of Medicine. He has been recognized with a number of awards, including the Damon Runyon Clinical Investigator Award (2016), the NIH Director’s New Innovator Award (2017), and the Mark Foundation Emerging Leader Award (2022). 

Lab News

Jaehyuk Choi, MD, PhD

Choi recruited to lead new Center for Cellular Therapies and Cancer Immunology

Jaehyuk Choi, M.D., Ph.D., a physician-scientist whose discoveries have transformed the field of cancer immunology, has begun his new role as the inaugural Director of the Center for Cellular Therapies and Cancer Immunology in the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. He also serves as Vice Chair for Translational Research and Innovation in the Department of Dermatology.

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Scientists say they have identified a root cause of lupus - one that could pave the way for new treatments

An imbalance of T cells, which play a key role in the body’s immune response, could explain most cases of the disease, according to new research.

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Stealing Strategies from Cancerous T Cells May Boost Immunotherapy

For some people with blood cancers like leukemia and lymphoma, CAR T-cell therapies have proven to be a transformative treatment. But for solid tumors like breast, colorectal, or pancreatic cancer, which make up about 90% of cancer cases, success with T-cell therapies has been harder to come by.

Select Publications

In vitro and in vivo screening identifies T cell mutations that reprogram CAR signalling and functional outputs.

Naturally occurring T cell mutations enhance engineered T cell therapies

T cell therapies have revolutionized cancer therapy for haematological cancers but have not yet been consistently effective in solid tumours, which represent 90% of adult cancers3. In both solid tumours and treatment-resistant haematological malignancies, they are limited by a combination of factors, including poor in vivo persistence, immunosuppressive environmental factors and T cell exhaustion4.

In vitro and in vivo screening identifies T cell mutations that reprogram CAR signalling and functional outputs.

Interferon subverts an AHR–JUN axis to promote CXCL13+ T cells in lupus

Systemic lupus erythematosus (SLE) is prototypical autoimmune disease driven by pathological T cell–B cell interactions1,2. Expansion of T follicular helper (TFH) and T peripheral helper (TPH) cells, two T cell populations that provide help to B cells, is a prominent feature of SLE.

Graphical model of immune checkpoint response in Merkel cell carcinoma. Courtesy of Zachary Reinstein.

Preexisting Skin-Resident CD8 and γδ T-cell Circuits Mediate Immune Response in Merkel Cell Carcinoma and Predict Immunotherapy Efficacy

Merkel cell carcinoma (MCC) is an aggressive neuroendocrine skin cancer with a ∼50% response rate to immune checkpoint blockade (ICB) therapy. In nonresponders, tumors show evidence of increased tumor proliferation, neuronal stem cell markers, and IL1. Responders have increased type I/II interferons and preexisting tissue resident (Trm) CD8 or Vδ1 γδ T cells that functionally converge with overlapping antigen-specific transcriptional programs and clonal expansion of public T-cell receptors.

Fig. 1: Loss of Pdcd1 enables oncogene-enforced glycolysis in T cells.

PD-1 instructs a tumor-suppressive metabolic program that restricts glycolysis and restrains AP-1 activity in T cell lymphoma

The PDCD1-encoded immune checkpoint receptor PD-1 is a key tumor suppressor in T cells that is recurrently inactivated in T cell non-Hodgkin lymphomas (T-NHLs). The highest frequencies of PDCD1 deletions are detected in advanced disease, predicting inferior prognosis.

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