Thomas Hägglöf, Ph.D.
- Assistant Professor, Department of Microbiology & Immunology
Area of research
- Lymphocytes, B cells, Tumor microenvironment, inflammation
Location
- Albert Einstein College of Medicine Jack and Pearl Resnick Campus 1300 Morris Park Avenue Forchheimer Building 416 Bronx, NY 10461
Research Profiles
Professional Interests
The Hagglof Lab – Exploring the Hidden Power of B Cells in Health and Disease
In the Hagglof Lab, we study one of the most fascinating but often underestimated components of the immune system: B cells. While B cells are well known for producing antibodies, they play a far more dynamic role in regulating immune responses, especially within diseased tissues.
Our research focuses on how B cells adapt and function in complex tissue environments, including inflamed tissues like tumors, fat during obesity, and sites of infection or vaccination. We explore how lymphocytes decide when to activate or when to suppress inflammation, and how they shape the body’s ability to fight disease or, in some cases, contribute to it.
To uncover these mechanisms, we use cutting-edge techniques such as genetic mouse models, advanced microscopy, high-dimensional flow cytometry, and sequencing. Our ultimate goal is to develop new strategies for immunotherapy by reprogramming B cell behavior in tissue-specific contexts.
Our lab sits at the intersection of immunology, cancer biology, metabolism, and translational medicine, and offers a highly collaborative, rigorous, and supportive training environment.
We’re always excited to welcome curious and driven lab members who want to ask bold questions about the immune system and pursue discoveries that could lead to the next generation of therapies.
Selected Publications
- Hägglöf T, Cipolla M, Loewe M, Chen ST, Mesin L, Hartweger H, ElTanbouly MA, Cho A, Gazumyan A, Ramos V, Stamatatos L, Oliveira TY, Nussenzweig MC, Viant C. Continuous Germinal Center Invasion Contributes to the Diversity of the Immune Response.
Cell. 2023 Jan
Antibody affinity maturation after infection or vaccination occurs in microanatomical structures called germinal centers (GC) by a mechanism that involves repeated cycles of somatic mutation and selection of GC B cells. We recently uncovered a key mechanism by which naïve B cells continuously enter previously established GCs to broaden the immune response – a process we termed GC invasion: https://www.cell.com/cell/fulltext/S0092-8674(22)01507-0 - Hägglöf T, Vanz C, Kumagai A, Dudley E, Ortega V, Siller M, Parthasarathy R, Keegan J, Koenigs A, Shute T, Leadbetter EA. T-bet+ B Cells Accumulate in Adipose Tissue and Exacerbate Metabolic Disorder During Obesity.
Cell Metabolism. 2022 Aug
We recently discovered that inflamed adipose tissue during obesity drives the expansion of B cells expressing the transcription factor T-bet, which contribute causally to systemic metabolic dysfunction by producing pathogenic IgG antibodies and orchestrating inflammation: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(22)00301-1 - Hägglöf T, Sedimbi SK, Yates JL, Parsa, R, Salas BH, Harris RA, Leadbetter EA, Karlsson MCI. Neutrophils license iNKT cells to regulate self-reactive mouse B cell responses.
Nature Immunol. 2016 Dec
We discovered an immune regulatory axis where neutrophils empower iNKT lymphocytes to safeguard against harmful autoreactive B cell responses, to establish a critical checkpoint during innate-driven immune activation that regulates autoantibody formation during sterile inflammation: https://www.nature.com/articles/ni.3583
Complete list of publications:
Pubmed: https://pubmed.ncbi.nlm.nih.gov/?term=thomas+hagglof&sort=pubdate&size=200
Google Scholar: https://scholar.google.com/citations?user=7wBYKBoAAAAJ&hl=en&oi=ao