Jacobson Lab research
About Associate Professor Kim Good-Jacobson
A/Prof Kim Jacobson (publishing as Kim Good-Jacobson) studies the formation of immunity. Human health and longevity is dependent on the ability of the immune system to clear the multitude of different foreign pathogens encountered over the life of the host. Her research studies the ability of the immune system to clear pathogens and form immunity through production of B cell memory.
A/Prof Jacobson leads the B cells and Antibody Memory laboratory at Monash University, investigating epigenetic modifiers underlying the formation of immune memory in health and chronic infection. She is a Bellberry-Viertel Fellow and former Victorian Young Tall Poppy Award recipient. A/Prof Jacobson completed her PhD at the Centenary and Garvan Institutes in 2007. She was awarded an Arthritis Australia AFA-ARA Heald Fellowship, followed by a CJ Martin Fellowship from the NHMRC to undertake postdoctoral training at Yale University, where she revealed a novel role for the inhibitory receptor PD-1 in humoral responses. She returned to Australia in 2010 and has since made key insights into how histone modifications regulate B cell memory, as well as discovering how antibody-secreting cells turn on the appropriate molecular program to migrate to their survival niche and provide lifelong protection. Her work has been published in Science, Nature Immunology and the Journal of Experimental Medicine. She recently served as Treasurer for the Australian and New Zealand Society for Immunology and has written for The Conversation.
1. Epigenetic regulation of immune memory.
2. Immune memory formation during chronic viral infection.
3. Targeting autoreactive antibody-secreting plasma cells for depletion.
Visit Associate Professor Good-Jacobson's Monash research profile to see a full listing of current projects.
Human health and longevity is dependent on the ability of the immune system to clear the multitude of different foreign pathogens encountered over the life of the host. Our research studies the ability of the immune system to clear pathogens and form immunity through production of B cell memory.
Progressive vaccine design and new therapeutics for B cell-derived cancers will rely on advances in our knowledge on the regulators that underpin B cell differentiation. Immune memory success relies on its adaptability: in response to different pathogens, variants of a single pathogen, and in balancing persistence with reactivation and terminal differentiation to plasma cells. This is likely achieved by producing a B cell memory population that is highly diverse.
There are three different themes of our research into immunity formed after immunisation or viral infection. We study:
(i) Formation of atypical and classical memory in chronic infectious diseases
(ii) Epigenetic regulation of memory B cell formation and responses
(iii) Targeting autoreactive antibody-secreting plasma cells for depletion
Revealing the individual roles of histone modifiers during the formation of immunity has the potential to reveal the molecular mechanisms underlying the production of a memory population that is able to persist in the absence of antigen whilst being poised to respond to subsequent infections. This not only has implications for vaccines and primary immunodeficiencies that are unable to produce memory cells, it will also result in a wider understanding of how epigenetic regulation controls gene expression programs during cell differentiation.
In sum, understanding the molecular networks and specific regulators that underpin B cell memory formation and function is core to finding new treatments for B cell-mediated disease and progressive vaccine design.
Epigenetic regulation of immunity
Immune memory induces faster and more efficient clearance of pathogen upon reinfection, vital for human health and longevity. Vaccines exploit this ability by providing the immune system the chance to form memory without exposure to a replicating pathogen. Memory B cells are generated during the initial response to infection, but persist long after the infection has cleared. Upon re-exposure, memory B cells rapidly proliferate and differentiate into high-affinity plasma cells, leading to a more efficient clearance of pathogen. Thus, memory B cells must balance long-term maintenance of the population with successful responses to one or more secondary infections.
Enzymes known as epigenetic modifiers can regulate cellular behaviour during an immune response by modulating the structure of the N-terminal tails of histones. These modifications induce or inhibit transcription of genes. In particular, there is growing evidence that epigenetic modifiers regulate lymphocyte development and responsiveness through dynamic changes in histone modifications. The role of epigenetic modifications in memory B cell development and function, however, is largely unknown. We recently provided evidence that epigenetic modifications are critical for memory B cell function (Good-Jacobson et al. 2014, PNAS). We are now continuing to investigate the role of epigenetic modifications during the formation of immunity in health and chronic infection.
Chronic infectious disease
Chronic infectious diseases have a devastating effect on global health. HIV and Plasmodium falciparum both cause chronic disease and have evaded effective vaccine design. Production and function of memory is altered in chronic infectious diseases, with recent work segregating memory B cells generated in chronic infection into classical memory and ‘atypical' memory B cell populations. However, the role of the latter is unclear, and whether atypical memory has a positive or negative impact on classical memory responses is controversial. It is clear that revealing the origin and function of these cells, and how their formation is regulated at the molecular level, will be important for development of new antibody-based vaccines for these diseases.
Immunity is of central importance to all organisms, as their very survival is dependent upon the ability to fight infection
and disease. Associate Professor Kim Jacobson and Professor Mariapia Degli-Esposti and are understanding how our
immune system identifies foreign invaders such as viruses and are paving the way in the development
of breakthrough treatments.
- Flow cytometry
- ELISAs & ELISpots
- VH sequencing
- Immunohistochemistry & immunofluorescence
- Conditional deletion models
- Tissue culture
- Lymphocytic choriomeningitis virus
- Helminth (Trichuris muris)
- Systemic lupus erythematosus
We collaborate with many scientists and research organisations around the world. Some of our more significant national and international collaborators are listed below. Click on the map to see the details for each of these collaborators (dive into specific publications and outputs by clicking on the dots).
Professor Stephen Turner
Professor Colby Zaph
Professor David Tarlinton
Associate Professor Stephanie Gras
Associate Professor Ian Cockburn (John Curtin School of Medical Research)
Dr Ian Parish (Peter MacCallum Cancer Centre)
Dr Joanna Groom (Walter + Eliza Hall Institute of Medical Research)
Dr Justin Taylor (Fred Hutchison Cancer Center, Seattle USA)
Dr Christopher Scharer (Emory University, Atlanta USA)
Student research projects
The Jacobson Lab offers a variety of Honours, Masters and PhD projects for students interested in joining our group. There are also a number of short term research opportunities available.
Please visit Supervisor Connect to explore the projects currently available in our Lab.