Forschungs- & Entwicklungsinformationsdienst der Gemeinschaft - CORDIS

Periodic Report Summary 1 - CD4INEAR (Defining the cellular interactions that control the retention of and tolerance induction in CD4 T cells at inflammatory sites)

The immune system is vital to protect us against pathogens. To achieve this, immune cells travel from lymphoid organs to sites of infection where they mediate pathogen clearance. Lymphocytes called CD4 T cells co-ordinate many different types of immune cell at both these sites. CD4 T cell are, therefore, central to most immune responses. This includes responses targeted at tissues of the body. Such responses can lead to autoimmune diseases, such as Rheumatoid Arthritis (RA), in which self-reactive CD4 T cells accumulate in inflamed tissues sites where they direct destructive responses painful joint damage.

Most current treatments for RA act by reducing all immune responses. This blanket immunosuppression can leave the host at risk of opportune infections. Moreover, these treatments do not cure the disease, they merely alleviate symptoms and, in the vast majority of cases, must be given for the life time of the individual. A more effective treatment strategy would be to remove the upstream mediators of the disease – the self-reactive CD4 T cells that co-ordinate the ongoing tissue damage.

To develop novel therapeutic approaches for inflammatory autoimmune diseases we need to know why CD4 T cells persist at sites of inflammation. To achieve this, an increased understanding of the characteristics and functions of CD4 T cells in peripheral tissues is required. Importantly, we need to investigate mechanisms by which self-reactive CD4 T cells can be silenced, removing these key drivers of destructive inflammation. This project will address these questions utilising cutting-edge techniques and novel research tools to generate important and original scientific research.

Reported by

United Kingdom


Life Sciences
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