CIHR supports important work on antibody response and immunity

CIHR supports important work on antibody response and immunity

The IRCM warmly congratulates Dr. Javier Di Noia and Dr. Tarik Möröy on their success in the spring 2023 CIHR grants.

Dr. Di Noia has been awarded nearly $850,000 over a five-year period to pursue his work entitled Molecular mechanisms underlying high-affinity and isotype switched antibody responses (Mechanisms that improve antibody quality), which explores immune mechanisms by focusing on a mutagenic enzyme called AID, which is expressed only in B lymphocytes, and whose complex role is still poorly understood. Indeed, AID must produce DNA damage, as a way to improve antibody quality, but this can as side effect that AID modifies other genes to predispose B cells to develop into lymphomas.

‘’We are studying the mechanisms that regulate AID activity, enabling an effective antibody response while minimizing collateral damage. For this project, we have carried out a large-scale study of proteins that could regulate AID activity and are pursuing promising candidates.’’ - Dr. Javier Di Noia

The research team has identified several candidates that regulate AID's ability to produce mutations at the level of antibody genes, but also elsewhere in the genome. Using B lymphocytes and mouse models of immunization, combined with biochemical and molecular biology techniques, the researchers aim to understand how these proteins regulate AID and their importance for antibody responses. 

Why this work is important

Exploiting these new mechanisms could lead to the design of better immunization strategies, as well as to identify defects in the proteins involved that could explain immunodeficiencies.

Dr. Tarik Möröy, meanwhile, has been awarded a one-year, $100,000 priority announcement for his work entitled The MYC/MIZ-1 complex in germinal center B cells and B cell lymphomagenesis (B cell maturation and B cell lymphoma). The primary aim of this work is to clarify the role of the transcription factors c-MYC and its cofactor MIZ-1 in the regulation of normal germinal center responses, including B cell proliferation, and to reveal how the deregulated expression of c-MYC and the c-MYC/MIZ-1 complex is responsible for the emergence and progression of B cell lymphoma.

Congratulations to both of them, and to all those who applied.

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