CCR7-dependent neutrophil trafficking as a driver of maladaptive T-cell activation in sterile injury and rheumatoid arthritis
Code: BC-DTP_2026_34
Title: CCR7-dependent neutrophil trafficking as a driver of maladaptive T-cell activation in sterile injury and rheumatoid arthritis
Primary Supervisor: Mathieu-Benoit VOISIN
Email: m.b.voisin@qmul.ac.uk
Institute: William Harvey Research Institute
Secondary Supervisor: Antal Rot
Email: a.rot@qmul.ac.uk
Institute: William Harvey Research Institute
Lay Summary:
Immune cell movement to different parts of the body is paramount during the development of a protective response against invading microorganisms. But it can also initiate self-destructive and excessive inflammatory diseases such as ischemia reperfusion injury (IRI) like stroke or heart attack and rheumatoid arthritis (RA), for which no cure have been found yet. Unfortunately, those two diseases have with higher proportion amongst East London communities. Targeting specific molecules controlling immune cell migration is therefore a realistic strategy to treat patients, especially those that do not respond well to available treatments. Amongst these key molecules is CCR7, that allows immune cells to enter specific organs named lymphatic ganglions where the harmful and self-destructive immune responses are initiated. Our study proposes to investigate how the molecule CCR7 is regulated in a specific immune cell, called neutrophils which is at the core of the aforementioned diseases. We will also investigate if targeting neutrophil-CCR7 can suppress disease development using pre-clinical lab models recapitulating the human disease. Ultimately, this project will provide a hitherto unexplored therapeutic avenue for controlling immune cell migration and hence their deleterious functions in pathologies with high prevalence in East London communities.
Aims:
Aim 1: To investigate the regulation of CCR7 in neutrophils (year 1)
Aim 2: investigate the impact of blocking neutrophil CCR7-dependent pathway for the establishment of acute and chronic inflammatory disorders (year 2 and 3)