David Withers

Reader in Cellular Immunology

University of Birmingham

United Kingdom

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About

David Withers is a Reader in Cellular Immunology at the University of Birmingham, UK. His research focuses on the roles of natural killer cells and innate lymphoid cells in cancer immunotherapy, as well as the dynamic changes within the tumor microenvironment. Recent publications include studies on tumor-infiltrating leukocytes, the modulation of immune responses, and the mechanisms behind T cell migration in relation to anti-tumor immunity.

Articles (17)

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2025

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2025

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2024

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2021

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2020

Collaborators (11)

Menno J. Oudhoff

NORWAY

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Belen Palencia

Clinica Universidad de Navarra

SPAIN

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Christopher Andrew Tibbitt

SWEDEN

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Ignacio Melero

SPAIN

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Zhi Li

University of Birmingham

UNITED KINGDOM

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Mengze Lyu

Weill Cornell Medicine

UNITED STATES

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Daniela Finke

Professor

University of Basel

SWITZERLAND

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Yohsuke Harada

University of Tokyo

JAPAN

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Peter Keane

Assistant Professor

University of Birmingham

UNITED KINGDOM

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Matthew Hepworth

The University of Manchester

UNITED KINGDOM

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Syed Murtuza Baker

The University of Manchester

UNITED KINGDOM

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David Withers

Research Interests

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Articles (17)

The Dark Side of NK Cells in Cancer Immunotherapy

Cellular Cosmetics: How Innate Lymphoid Cells Can Recontour the Tumour Microenvironment

Dynamic Tracking of Tumor Microenvironment Modulation Using Kaede Photoconvertible Transgenic Mice Unveils New Biological Properties of Viral Immunotherapy

Rapid functional impairment of natural killer cells following tumor entry limits anti-tumor immunity

Tumour-retained activated CCR7+ dendritic cells are heterogeneous and regulate local anti-tumour cytolytic activity

Decoding changes in tumor‐infiltrating leukocytes through dynamic experimental models and single‐cell technologies

Protocol for transcutaneous tumor photolabeling to track immune cells in vivo using Kaede mice

Migration of stem-like CD8 T cells between tissue microenvironments underpins successful anti-tumour immune responses

Bcl6 is a subset-defining transcription factor of lymphoid tissue inducer-like ILC3

Inhibitory IL-10-producing CD4<sup>+</sup> T cells are T-bet-dependent and facilitate cytomegalovirus persistence via coexpression of arginase-1

ILC killer: Qu’est-ce que c’est?

Reciprocal transcription factor networks govern tissue-resident ILC3 subset function and identity

Dysregulation of ILC3s unleashes progression and immunotherapy resistance in colon cancer

T-bet and RORα control lymph node formation by regulating embryonic innate lymphoid cell differentiation.

Stable Epigenetic Programming of Effector and Central Memory CD4 T Cells Occurs Within 7 Days of Antigen Exposure <i>In Vivo</i>.

Acetylcholine production by group 2 innate lymphoid cells promotes mucosal immunity to helminths.

IL‐2/IL‐7‐inducible factors pioneer the path to T cell differentiation in advance of lineage‐defining factors

Collaborators (11)

Menno J. Oudhoff

Belen Palencia

Christopher Andrew Tibbitt

Ignacio Melero

Zhi Li

Mengze Lyu

Daniela Finke

Yohsuke Harada

Peter Keane

Matthew Hepworth

Syed Murtuza Baker

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