Our central goal is to understand the mechanisms by which B-cells diversify their genome to elicit a protective immune response against pathogens. We are particularly interested in how this process, called antibody diversification, can lead to the formation of hematological cancers, including lymphoma, leukemia, and multiple myeloma.
B-cells are central components of the adaptive immune response and play a key role in protecting humans from infections by producing antibodies. These proteins can bind and neutralize pathogens, including bacteria, viruses, and parasites. Antibodies are encoded by a limited set of genes called Immunoglobulin genes and we face a major challenge: how can we produce enough antibodies to eliminate the expanding spectrum of pathogens with only a limited amount of genetic information?
B-cells use a unique and formidable mechanism, named antibody diversification to counteract this issue. It requires the formation of programmed DNA lesions in the Immunoglobulin genes, in particular, DNA double-strand breaks, to favour genetic diversity. When this mechanism is non-functional, it can result in immunodeficiency syndromes and recurrent infections. Unfortunately, this process can also trigger genomic rearrangements, for instance, chromosomal translocations that fuel the formation of B-cell cancers.
We are particularly interested in:
- Elucidating how DNA double-strand breaks are repaired in B-cells to allow for a protective immunity but limit B-cell carcinogenesis.
- Identifying new markers for the diagnosis of B-cell malignancies and immunodeficiency syndromes as well as defining novel targets for the treatment of patients affected by these diseases.
Our ultimate goal to provide better care for patients affected by haematological malignancies and immunodeficiency syndromes. If this area of research interests you, feel free to contact us to find out how you could help.