Dr David Withers PhD

Dr David Withers

Institute of Immunology and Immunotherapy
Wellcome Trust Research Fellow

Contact details

Institute of Immunology and Immunotherapy
College of Medical and Dental Sciences
University of Birmingham
B15 2TT

David Withers is a Wellcome Trust funded Research Fellow

Research in the Withers Lab is focused on understanding how memory CD4 T cell responses are generated and maintained. At present we are particularly interested in the role of RORgt-expressing group 3 Innate Lymphoid Cells within secondary lymphoid tissue.


  • PhD Immunology 2004
  • BSc (Hons) Microbiology and Virology 2000


David Withers qualified with a BSc (Hons) in Virology and Microbiology from the University of Warwick in 2000. He went on to study for a PhD in Immunology at the Institute for Animal Health in conjunction with the University of Bristol. After obtaining his PhD, David continued his studies in the laboratory of Peter Lipsky at NIAMS, NIH, Bethseda (2004-2006). He then returned to the UK to study with Peter Lane at the University of Birmingham, cementing his interest in secondary lymphoid tissue development/structure and how this controlled CD4 T cell responses. Research in the Withers Lab is supported by the Wellcome Trust. In 2011 he was awarded a Wellcome Trust Research Career Development Fellowship to establish his own research group investigating the role of lymphoid tissue inducer cells in lymph nodes. In 2016 he was awarded a Wellcome Trust Senior Research Fellowship in Basic Biomedical Science.


Teaching Programmes

Postgraduate supervision

 The Withers Lab is currently full for PhD students.



T cell responses, Innate Lymphoid Cells, Immunological memory


David’s research is focused on understanding the signals involved in the development and maintenance of T cell responses, in particular, the development of memory CD4 T cells which are essential for immunological memory and thus vaccination. Understanding how memory CD4 T cells are generated and maintained is crucial for improving our ability to enhance vaccination, but also potentially to modulate unwanted self-reactivity. Key areas of research:

ILC3 control of CD4 T cell responses

Multiple studies indicate that ILC3, the RORgt-expressing population of Innate Lymphoid Cells, modulate CD4 T cells at different stages of the response. Using established models to track endogenous antigen-specific T cell responses, we are dissecting the role of ILC3 and mechanisms they use, in the regulation of CD4 T cell responses.

ILC3 biology in health and disease

Much of the basic biology of ILC3 remains poorly understood. We are assessing their location, migration and activation in vivo in both murine and human tissues to better understand this cell population

Regulation of ILC3 function

Recently we have developed a series of tools to determine the role of key transcription factors in controlling ILC3 function, an exciting new area of study that is revealing key information in the transcriptional regulation of ILC3 functions and may provide clues to how to manipulate these cells.


Marriott CL, Carlesso G, Herbst R and Withers DR (2015) ICOS is required for the generation of both central and effector CD4(+) memory T-cell populations following acute bacterial infection. Eur J Immunol 45(6):1706-15

Mackley EC, Houston S, Marriott CL, Halford EE, Lucas B, Cerovic V, Filbey KJ, Maizels RM, Hepworth MR, Sonnenberg GF, Milling S and Withers DR (2015) CCR7-dependent trafficking of RORγ⁺ ILCs creates a unique microenvironment within mucosal draining lymph nodes. Nat Commun 6:5862

Marriott CL, Mackley EC, Ferreira C, Veldhoen M, Yagita H and Withers DR (2014) OX40 controls effector CD4+ T-cell expansion, not follicular T helper cell generation in acute Listeria infection. Eur J Immunol 44(8):2437-47

Withers DR, Gaspal FM, Mackley EC, Marriott CL, Ross EA, Desanti GE, Roberts NA, White AJ, Flores-Langarica A, McConnell FM, Anderson G and Lane PJ (2012) Cutting edge: lymphoid tissue inducer cells maintain memory CD4 T cells within secondary lymphoid tissue. J Immunol 189(5):2094-8

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