BSI Manchester Immunology Group Seminar Series: Dr Damian Perez Mazliah, University of York. Location: MS Lecture Theatre, Michael Smith Building
| Dates: | 10 April 2025 |
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| Times: | 12:00 - 13:00 |
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| What is it: | Seminar |
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| Organiser: | School of Biological Sciences |
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| How much: | Free |
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| Who is it for: | University staff, Adults, Alumni, Current University students |
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| Speaker: | Damian Perez Mazliah |
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Talk entitled "B cell immunity during infectious heart disease"
Brief Bio
Dr. Damian Perez Mazliah is a Biologist specialised in immunology, infection and parasitology, with expertise in malaria and trypanosomiasis. He completed his PhD at the National Institute for Parasitology, Buenos Aires, Argentina, where he studied T cell immunity to trypanosoma parasites. He then moved to the National Institute for Medical Research, Mill Hill, London, UK (later the Francis Crick Institute) where he completed a postdoc looking at B cell immunity to malaria. Later, he moved to The Lancet where he worked as a Senior Editor for EBioMedicine (part of The Lancet Discovery). Damian joined the Medical School from the University of York in 2019
as an Independent Research Fellow and became a Principal Investigator in 2022 funded by the Royal Society. His laboratory based at York is currently focusing on immunity to protozoan parasites, autoimmunity and cardioimmunology. Web: https://www.hyms.ac.uk/about/people/damian-perez-mazliah
Abstract
B cell immunity during infectious heart disease
Although the triggers for autoimmune disorders are diverse and, in many cases, unknown, some pathogens have the outstanding capacity to alter our immune system leading to malfunctioning and autoimmunity. Our laboratory is currently exploring the mechanisms that regulate infection driven autoimmunity, particularly focusing on infection-driven heart disease. Cardiovascular diseases are the leading cause of death globally. The immune system plays a key role in cardiac development, composition, and function. Under some circumstances, particularly in response to infection, immune cells can infiltrate the heart in large numbers to remove dying tissue,
scavenge pathogens and promote healing. If uncontrolled, these immune cells can cause collateral tissue damage, leading to heart dysfunction and failure. Moreover, the heart can be directly affected by autoreactive B cells, resulting in damage to its structures. Our goal is to better understand how the B cells that fight infections and those that attack the heart develop, and to identify the cellular and molecular mechanisms through which autoreactive B cells contribute to heart tissue damage. For this, we are using Trypanosoma cruzi as an infection model. T. cruzi is the protozoan parasite that causes Chagas disease (American trypanosomiasis), a major cause of infectious heart disease worldwide and the highest-impact parasitic disease in the Western Hemisphere. In response to T. cruzi infection/Chagas disease, and driven by poorly understood triggers, the immune system produces both antibodies against the parasite and against the body’s heart. Using a combination of molecular and cellular
technologies (scRNA-seq, spatial transcriptomics, RNAScope, flow cytometry) we have now identified that chronic T. cruzi infection leads to a large and very unusual accumulation of B cells in the heart. During the talk, I will discuss our most recent datasets studying the immune response during experimental Chagas heart disease. I will also discuss our plans for studying the nature of these heart-resident B cells, how do they interact with other types of heart-resident cells (e.g. fibroblasts, cardiomyocytes) and ultimately, whether and how do they contribute to development of heart fibrosis and/or dilated cardiomyopathy.
Speaker
Damian Perez Mazliah
Organisation: University of York
Travel and Contact Information
Find event
Michael Smith Lecture Theatre
Michael Smith Building
Manchester
