T cells are a critical part of the immune system. Their role is to patrol the blood and tissues in order to detect and eliminate virus-infected and cancer cells. In the Hudson lab, we seek to understand T cell biology and improve their function, with the goal of developing new therapies against infections, autoimmunity, and cancer.
The Hudson lab is located in the Texas Medical Center in Houston, Texas. We are part of Baylor College of Medicine’s Department of Molecular and Cellular Biology and the Dan L. Duncan Comprehensive Cancer Center.
T cells are responsible for destroying tumors and cells infected with intracellular pathogens such as viruses and bacteria. Unfortunately T cell responses are not always optimal, leading to chronic infections and the growth of tumors.
Our research focuses on understanding the causes of T cell dysfunction in order to develop new immunotherapies for cancer and other diseases.
T cell exhaustion
“Exhaustion” is the process by which T cells become dysfunctional and fail to control tumors and infections. By understanding the biology of T cell exhaustion, we can identify new targets and strategies to improve T cell function. Our research focuses on identifying signals that inhibit T cell function and can be targeted for new immunotherapies.
Immunotherapies – modification of the immune system to treat diseases – have revolutionized the treatment of cancer. Unfortunately, not all patients respond to current immunotherapies. We seek to identify new strategies and drugs to improve T cell responses in patients with cancer and infectious disease.
Immunology method development and application
In recent years, new tools have emerged that permit incredible and detailed study of biological systems. We develop, refine, and apply these methods to immunological questions, allowing unprecedented insight into T cell development and function.
Deep mutational scanning identifies SARS-CoV-2 Nucleocapsid escape mutations of currently available rapid antigen tests
Distinct phenotypic states and spatial distribution of CD8 + T cell clonotypes in human brain metastases.
Proliferating Transitory T Cells with an Effector-like Transcriptional Signature Emerge from PD-1+ Stem-like CD8+ T Cells during Chronic Infection
We gratefully acknowledge the support of:
October 11, 2022
Research presentation at 10x Genomics Spatial Biology Symposium
We recently presented our work on spatial T cell receptor sequencing at the 10x Genomics Spatial Biology Symposium in Boston! You can check out the recording on demand here.
October 06, 2022
Perspective article published in Cancer Cell
We have a new publication in Cancer Cell! In this perspective article, we discuss the role of various -omics technologies in studying T cells within the tumor microenvironment. In particular, we focus on the opportunities these techniques present to deepen our understanding of T cell biology and also describe the challenges that arise in the interpretation and analysis of these experiments.
August 26, 2022
New paper: mapping escape mutations to SARS-CoV-2 antigen tests
Our work describing a new assay for antibody epitope mapping was published today in Cell. This work was a collaboration with the Ortlund Lab at Emory University.
New SARS-CoV-2 mutations are emerging continually, threatening not only to evade immune responses but also to escape binding of antibodies used in antigen tests (also known as rapid tests) to detect COVID-19 infection. In this work, we describe a new method to identify SARS-CoV-2 mutations that escape commonly-used antigen tests.
Most antigen tests detect the SARS-CoV-2 nucleoprotein. To map epitopes of anti-nucleoprotein antibodies, we induced nucleoprotein expression on the surface of cells by adding a secretion leader sequence to the N-terminus and a transmembrane domain to the C-terminus. We then created a deep mutational library that expressed every possible single nucleoprotein mutation. By incubating this library of surface-expressed nucleoprotein with antibodies used in rapid tests and sorting cells without antibody binding, we could identify every single mutation that eliminated nucleoprotein detection by rapid test antibodies.
The results from this assay showed that current variants of concern are unlikely to evade currently-available antigen tests. Additionally, these data provide a useful resource for predicting the detectability of future SARS-CoV-2 variants with antigen tests. Finally, this method is generalizable to map interaction and functional surfaces of proteins in a wide variety of contexts.