Summary
IgG4-autoimmune diseases (IgG4-AID) are rare but collectively correspond to a significant group of devastating diseases affecting
many different organs, e.g. skin, brain, nerves and kidney in patients that often remain unresponsive to current treatments. IgG4-AID
have commonalities indicating a shared underlying immunopathogenesis that make a joint approach to identify new therapeutic
targets and test new treatment strategies feasible and necessary. We hypothesize that genetic risk factors and a dysregulated
immune response may lead to an increased susceptibility to produce antibodies targeting self-proteins. These are of a special
subclass called IgG4, which are usually harmless but can cause disease in these patients by interfering with normal functions in the
body. We are the first consortium that aims to study IgG4-AID comparatively, including pathogenic IgG4, and the cells, molecules and
mechanisms involved in IgG4 autoantibody production, using an explorative multi-omics approaches in combination with state-ofthe-
art cell and molecular biology methodology. We will establish a new humanized mouse model of IgG4-AID for the development
and testing of a novel immune-apheresis based therapy aimed as immediate relief therapy for all IgG4-AID patients. Our innovative
training program combines university-based and multidisciplinary research-based training with state-of the art web-based training
and in-person trainings by the academic and non-academic sector. We aim to foster a new generation of experts in IgG4-AID that are
1) are highly employable both in the academic and industry sectors and qualified for innovative multidisciplinary translational
research with a focus on biomedical product development and 2) equipped with the skillsets for digitalization, awareness for gender
equality and diversity and competent in sustainable research and innovation approaches to address current and future challenges,
such as climate change, social inequalities and pandemics.
many different organs, e.g. skin, brain, nerves and kidney in patients that often remain unresponsive to current treatments. IgG4-AID
have commonalities indicating a shared underlying immunopathogenesis that make a joint approach to identify new therapeutic
targets and test new treatment strategies feasible and necessary. We hypothesize that genetic risk factors and a dysregulated
immune response may lead to an increased susceptibility to produce antibodies targeting self-proteins. These are of a special
subclass called IgG4, which are usually harmless but can cause disease in these patients by interfering with normal functions in the
body. We are the first consortium that aims to study IgG4-AID comparatively, including pathogenic IgG4, and the cells, molecules and
mechanisms involved in IgG4 autoantibody production, using an explorative multi-omics approaches in combination with state-ofthe-
art cell and molecular biology methodology. We will establish a new humanized mouse model of IgG4-AID for the development
and testing of a novel immune-apheresis based therapy aimed as immediate relief therapy for all IgG4-AID patients. Our innovative
training program combines university-based and multidisciplinary research-based training with state-of the art web-based training
and in-person trainings by the academic and non-academic sector. We aim to foster a new generation of experts in IgG4-AID that are
1) are highly employable both in the academic and industry sectors and qualified for innovative multidisciplinary translational
research with a focus on biomedical product development and 2) equipped with the skillsets for digitalization, awareness for gender
equality and diversity and competent in sustainable research and innovation approaches to address current and future challenges,
such as climate change, social inequalities and pandemics.
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More information & hyperlinks
Web resources: | https://cordis.europa.eu/project/id/101119457 |
Start date: | 01-09-2023 |
End date: | 31-08-2027 |
Total budget - Public funding: | - 2 626 812,00 Euro |
Cordis data
Original description
IgG4-autoimmune diseases (IgG4-AID) are rare but collectively correspond to a significant group of devastating diseases affectingmany different organs, e.g. skin, brain, nerves and kidney in patients that often remain unresponsive to current treatments. IgG4-AID
have commonalities indicating a shared underlying immunopathogenesis that make a joint approach to identify new therapeutic
targets and test new treatment strategies feasible and necessary. We hypothesize that genetic risk factors and a dysregulated
immune response may lead to an increased susceptibility to produce antibodies targeting self-proteins. These are of a special
subclass called IgG4, which are usually harmless but can cause disease in these patients by interfering with normal functions in the
body. We are the first consortium that aims to study IgG4-AID comparatively, including pathogenic IgG4, and the cells, molecules and
mechanisms involved in IgG4 autoantibody production, using an explorative multi-omics approaches in combination with state-ofthe-
art cell and molecular biology methodology. We will establish a new humanized mouse model of IgG4-AID for the development
and testing of a novel immune-apheresis based therapy aimed as immediate relief therapy for all IgG4-AID patients. Our innovative
training program combines university-based and multidisciplinary research-based training with state-of the art web-based training
and in-person trainings by the academic and non-academic sector. We aim to foster a new generation of experts in IgG4-AID that are
1) are highly employable both in the academic and industry sectors and qualified for innovative multidisciplinary translational
research with a focus on biomedical product development and 2) equipped with the skillsets for digitalization, awareness for gender
equality and diversity and competent in sustainable research and innovation approaches to address current and future challenges,
such as climate change, social inequalities and pandemics.
Status
SIGNEDCall topic
HORIZON-MSCA-2022-DN-01-01Update Date
31-07-2023
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