Jukka
Alinikula
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Areas of expertise
Biography
I completed my PhD with Prof. Olli Lassila at the University of Turku, where I studied the transcriptional regulation of B-cell and plasma-cell development. During my postdoctoral training with Prof. David G. Schatz at Yale University (2012–2015), I investigated the mechanisms that target somatic hypermutation to immunoglobulin genes.
I established my research group at the Institute of Biomedicine, University of Turku, shortly thereafter. Our work focuses on understanding how B cells generate protective antibody responses and how the mutational mechanisms that optimize antibody function can also contribute to cancer development.
In addition to leading an independent research team, I serve as University Lecturer in Immunology and Drug Development. My research combines molecular immunology, genomics, genome engineering and single-cell approaches to study antibody diversification, infection immunity and lymphomagenesis.
Teaching
My teaching focuses on immunology and immunopharmacology across Bachelor's, Master's, MD, and doctoral programmes in both English and Finnish.
I employ a range of teaching methods, including lectures, case-based learning, journal clubs, laboratory courses, mentoring, thesis supervision, and online learning. My teaching covers innate and adaptive immunity, immunomodulatory drugs, therapeutic antibodies, and protein-based therapeutics.
I have completed university pedagogy studies and actively supervise doctoral researchers. In addition, I serve on the follow-up committees of PhD students and contribute to the development of undergraduate, postgraduate, and doctoral education.
Research
Protective immunity depends on germinal center B cells that generate high-affinity, class-switched antibodies during infection and in response to vaccination. We investigate the molecular mechanisms that enable these antibody responses and establish long-term humoral immunity.
A major focus of our research is somatic hypermutation (SHM), a specialized mutational process that diversifies immunoglobulin genes and drives antibody affinity maturation. While most cells minimize mutations to preserve genome stability, germinal center B cells deliberately mutate their antibody genes to improve antigen recognition. We aim to understand how SHM is targeted with high specificity to immunoglobulin genes and how this process is regulated across the genome.
Our work seeks to uncover the molecular rules that determine why some genomic regions are highly mutable while others remain protected. We are particularly interested in the roles of transcription, gene regulation and genome organization in directing SHM activity. These studies provide insight into fundamental mechanisms underlying antibody diversification and adaptive immunity.
Because SHM relies on DNA mutagenesis, errors in targeting can have severe consequences for genome integrity. Off-target mutations contribute to the development of lymphoma and other malignancies, making SHM both a key mechanism of protective immunity and an important source of cancer-associated mutations. We therefore also investigate how mutational processes become mis-targeted to proto-oncogenes, other genomic loci and viral genomes.
To address these questions, we combine molecular immunology, functional genomics, genome engineering, reporter systems, high-throughput sequencing and single-cell technologies to uncover the principles that govern antibody diversification, mutation targeting and disease.