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Glycans as Master Switches of B Cell Activity in Autoimmunity

Project description

The role of glycosylation in autoimmune diseases

Glycosylation is a post-translational modification process that involves the addition of sugar molecules to proteins. In the immune system, glycosylation plays an essential role in regulating the interactions between immune cells and their environment. In the case of antibodies, glycosylation at the fragment antigen-binding (Fab) region affects the antigen-binding affinity of antibodies and may lead to the development and progression of autoimmune diseases. The ERC-funded GlycanSwitch project aims to investigate the cellular mechanisms underlying Fab glycosylation and its effects on the immune system. Researchers will focus on the glycosylation of the B cell receptor and its role in the selection and activation of autoreactive B cells. Project findings will provide the groundwork for targeted therapies against autoimmunity.

Objective

Autoimmune diseases including rheumatoid arthritis (RA) are often life-threatening disorders with increasing disability having a negative impact on patients’ quality of life. Mechanisms leading to the breach of tolerance in development of autoimmunity are still largely unknown. Protein glycosylation is an essential regulatory mechanism in the immune system. We recently demonstrated that N-glycosylation of the variable region (Fab) of autoantibodies is a hallmark of RA development and progression. We also demonstrated that autoantibodies acquire these Fab glycosylation signatures already many years before disease onset. We herein hypothesize that Fab glycosylation at the level of the B cell receptor is a key molecular switch promoting the selection, activation and proliferation of autoreactive B cells leading to the concomitant breach of immunotolerance. Within GlycanSwitch, we will map the Fab glycome of various types of RA autoantibodies and autoreactive B cells. We will study the factors and underlying cellular mechanisms that regulate Fab glycosylation of B cell receptors and autoantibodies. We will investigate the immunological effects of Fab glycosylation and the impact in B cells signalling and activation in the context of molecular and cellular interacting partners in the immune microenvironment. Finally, we will test in relevant mouse models how Fab glycosylation of autoantibodies and autoreactive B cells contributes to the breach of tolerance. We expect that the obtained insights into the role of glycans as key checkpoint for the selection of autoreactive B cells and the rise of autoimmunity will provide leads for targeted therapeutic interventions as well as rationales for the early detection of RA and autoimmune diseases in general. We foresee that the knowledge generated will allow us to embark on a targeted prevention clinical study in patients at risk for RA to turn off the GlycanSwitch leading to chronic RA.

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HORIZON-ERC-SYG - HORIZON ERC Synergy Grants

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Call for proposal

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(opens in new window) ERC-2022-SYG

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Host institution

ACADEMISCH ZIEKENHUIS LEIDEN
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 5 000 000,00
Address
ALBINUSDREEF 2
2333 ZA Leiden
Netherlands

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Activity type
Higher or Secondary Education Establishments
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Total cost

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€ 5 000 000,00

Beneficiaries (4)

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