
Links
Areas of expertise
Biography
I completed my PhD with Prof. Olli Lassila at the University of Turku, focusing on the transcriptional regulation of B cell and plasma cell development and function through loss-of-function studies. During my postdoctoral research at Yale Immunobiology (USA) with David G. Schatz (2012–2015), I investigated the targeting of somatic hypermutation to immunoglobulin genes.
Shortly thereafter, I established my own research group at the Institute of Biomedicine, University of Turku, Finland. In addition to leading independent research projects, I serve as a university lecturer in immunology and drug development.
Teaching
Teaching focus ares:
- Immunology
- Immunopharmacology
I teach accrioss various Bachelor's, Master's, MD, and PhD courses in both English and Finnish. My teaching methods include lectures, case-based learning, journal clubs, mentoring, laboratory courses, thesis supervision, and online courses. The topics I cover span innate and adaptive immunity, immunomodulatory drugs and therapeutic antibodies and proteins. I have completed courses on university pedagogy and have supervised and continue to supervise PhD students. Additionally, I participate in follow-up committees of doctoral students.
Research
Protective immunity requires the production of high-affinity antibody-producing cells. My team and I study how high-affinity antibody production is achieved. While most cells minimize somatic mutations to preserve genome stability and prevent tumorigenesis, immunoglobulin genes in B cell development are actively mutated. For example, germinal center B lymphocytes undergo somatic hypermutation (SHM) of immunoglobulin V regions.
Failure to correctly target these mutations can have severe consequences for genome integrity and is implicated in several forms of cancer, particularly leukemia and lymphoma. My research focuses on investigating the molecular mechanisms by which immunoglobulin enhancers recruit SHM to immunoglobulin genes, as well as the processes that lead to the mis-targeting of mutations to other sites in the genome, including several proto-oncogenes.
To address these questions, we utilize techniques such as reporter assays, library screening, genome manipulation, and whole-genome analysis.