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Decreased levels of oxygen radicals cause autoimmune disease.

April 11, 15:15 - 16:15

Organizer

The Svedberg Seminar Series
thesvedberg@scilifelab.uu.se
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Venue

Navet, SciLifeLab, Uppsala
SciLifeLab Uppsala, BMC (Entrance: C11), Husargatan 3,
Uppsala, 75237 Sweden
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Decreased levels of oxygen radicals cause autoimmune disease.

April 11, 2022 @ 15:15 16:15 CEST

Prof. Rikard Holmdahl 

Karolinska Institute, Sweden

Rikard Holmdahl made his PhD (1985) and MD (1987) at Uppsala University. Professor in medical inflammation research Lund University 93-07. Professor at Karolinska Institute from 2008

Venue: Hybrid meeting – Trippelrummet, Navet and zoom

SciLifeLab Uppsala, BMC (Entrance: C11), Husargatan 3,
Uppsala, 75237 Sweden
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View Venue Website

Title of the seminar: Finding and understanding genes associated with common diseases; decreased levels of oxygen radicals cause autoimmune disease

A long-standing challenge is to understand which genes that cause common complex diseases, such as rheumatoid arthritis, atherosclerosis or cancer, and thereby understand the disease causes. However, even though we know the human sequence and can genotype millions of individuals it is very difficult to conclusively identify the single nucleotide variants that cause the diseases. We have taken another approach through animal models. Both genetics and diseases show similarities with humans, and we have shown that it is possible to not only identify the loci associated with disease but also exactly position the polymorphic nucleotides for common autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). 

I will focus on the first gene that we cloned, Ncf1, which regulate immune tolerance through different levels of oxygen radicals, or more precisely hydrogen peroxide. It is the major gene causing SLE and is important in Sjögren’s syndrome and RA and most likely most autoimmune disease.

To understand the role of Ncf1 is also complicated as peroxide seem to regulate many different pathways leading to autoimmune diseases. I will discuss how we think it regulates RA and SLE but also how it could explain our normal behaviour, thus explaining why Ncf1 variants are common in both rat and human population.

Read more about ikard Holmdahl´s research http://ki.se/en/mbb/research-division-of-medical-inflammation-research