Costimulatory signals are critical for the success of T cell responses. For CD4 Th1 effector and memory responses, OX40 signals are essential, however, our understanding of the key cellular sources of OX40L in vivo, alongside how expression of OX40L is regulated, is lacking. Here we demonstrate that provision of OX40L by DC, but not T cells, B cells nor ILC3 is required and determine how DC expression of OX40L is regulated through cross-talk with NK cells. We then contrast cellular provision of OX40L in systemic Th1 responses with the requirments for Th17 responses in the intestine.
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.