The Hudson Laboratory

We are thrilled to announce that the Hudson Lab has been awarded a five-year R01 grant from the National Institute of Allergy and Infectious Diseases (NIAID) to study how the surface receptor CD7 regulates exhausted CD8+ T cells!

This award – titled “Regulation of exhausted T cell responses by CD7” – builds directly on our lab’s recently published work in Cell Reports, in which we identified CD7 as a previously unrecognized survival receptor that protects exhausted CD8+ T cells from programmed cell death during chronic infection and cancer.

Exhausted CD8+ T cells arise when the immune system faces prolonged threats – such as cancer or chronic viral infection – and gradually lose their ability to persist and kill target cells. While much attention has focused on re-awakening exhausted T cells through immune checkpoint blockade, far less is known about what keeps these cells alive in the first place. Our prior work showed that CD7 plays a central role in that survival – and that its loss leads to the collapse of antigen-specific T cell populations and impaired disease control.

This grant will allow us to go much deeper. Over the next five years, we will define the molecular mechanisms by which CD7 regulates T cell survival and effector function, determine its importance for controlling chronic viral infection and tumors in vivo, and test whether boosting CD7 signaling can improve the persistence and effectiveness of engineered T cell therapies, including CAR T cells. We are incredibly grateful to NIAID for their support of this work, and we are excited about what the next five years will bring!

We are thrilled to congratulate graduate student Amanda Xia on being awarded an F30 fellowship grant from the National Institute of Allergy and Infectious Diseases (NIAID) to support her doctoral research. Amanda is a student in Baylor’s MD/PhD program, and this four-year, $198,000 award will fund her investigation into how CD8+ T cells – the immune system’s front-line killers of virus-infected and tumor cells – carry out their work, and how that process breaks down in chronic settings like long-term viral infections and cancer.

When the immune system faces a persistent threat, CD8+ T cells can lose their ability to effectively eliminate infected or cancerous cells – a process known as exhaustion. Amanda’s research aims to uncover the molecular mechanisms that drive this loss of function, with the goal of identifying new ways to restore or enhance T cell killing capacity. A deeper understanding of these processes could open new doors for improving immunotherapy outcomes for patients with chronic infections and cancer.

We are incredibly proud of Amanda and grateful to NIAID for their support of this work!

We are thrilled to share that our lab’s work on spatially resolved T cell profiling in head and neck cancer has been published in Science Immunology!

In this study, led by postdoctoral scientist Dr. Kelli McCord, we developed a new approach to visualize where specific T cell clones are located within tumors – at single-cell resolution – and applied it to head and neck squamous cell carcinoma (HNSCC), a disease responsible for nearly 400,000 deaths each year that remains difficult to treat with immunotherapy.

To do this, we combined high-parameter spectral flow cytometry and single-cell RNA and TCR sequencing on 27 patients with HNSCC. We then used the Xenium spatial transcriptomics platform and designed patient-specific probes targeting individual T cell receptor sequences, allowing us to map the precise location of specific T cell clones while simultaneously measuring their gene expression in intact tumor tissue.

Our results revealed that T cells with more robust cancer-fighting potential clustered in immune-rich niches, while exhausted T cells were more broadly dispersed in tumor-dense regions. Strikingly, cells sharing the same T cell receptor — and therefore recognizing the same target — could adopt fundamentally different functional states depending on where they were located in the tumor. This spatial heterogeneity was not captured by conventional approaches like flow cytometry or single-cell RNA sequencing alone, suggesting that local environmental cues in the tumor — not clonal identity alone — play a dominant role in shaping T cell fate. They also reveal substantial differences in immune architecture across patients that may help explain why some respond to immunotherapy while others do not.

We are particularly grateful to our clinical collaborators, to the patients who donated samples, and to the many core facilities and funding sources that made this work possible.