November 10-15

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ACR Convergence 2023

San Diego, CA

Home // Chris Wincup, MBChB, MRCP: SLE and links to iron deficiency, mitochondrial dysfunction

Chris Wincup, MBChB, MRCP: SLE and links to iron deficiency, mitochondrial dysfunction


3 minutes

Poster presenter: Chris Wincup, MBChB, MRCP, clinical research fellow, University College London

Poster title: Tired T-Cells and Monocytes with Malaise: Investigating the Links Between Cellular Iron Deficiency and Mitochondrial Dysfunction in Systemic Lupus Erythematosus

Scheduled poster session day and time: Friday, Nov. 6, 9 – 11 a.m. EST

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What is your poster about?

At the 2019 annual meeting, I presented data showing that patients with SLE are at risk of Functional Iron Deficiency. This is a state in which there is an abundant supply of iron within the body, but it cannot be released from stores or transported at an adequate rate to meet cellular demands. Iron is an essential mineral for several vital physiological processes, most obviously in erythrocyte development, but also in maintaining healthy mitochondrial function. I’ve found that healthy immune cells grown in iron-deficient conditions display impaired mitochondrial ATP generation. The work I’m presenting this year is the next step in this study, in which I sought to identify if immune cells from patients with SLE were iron deficient and whether this impacted their mitochondrial function. T-cells and monocytes were taken from patients with SLE and healthy controls, and I then investigated for cellular features of iron deficiency by flow cytometry and measured mitochondrial respiration via the Seahorse technique. 

Why did you decide to investigate this topic?

This research project started almost three years ago and was initially based upon our interesting observation that red cell distribution width (a surrogate marker of functional iron deficiency) correlated with fatigue scores in three large cohorts of patients with SLE. Fatigue is a major problem for SLE patients, and we do not have any reliable treatments for this in many cases, which makes this a significant unmet need. I hypothesized that this state of cellular iron deficiency may result in impaired mitochondrial ATP production in immune cells and that this could potentially be an avenue to identifying new therapeutic options in SLE that could also potentially improve fatigue.

What excites you most about your work?

There have been some huge advances in our understanding of the pathogenesis of SLE over recent decades, and this has ultimately led to the development of new treatment options, so it’s a really interesting time to be doing research in lupus. It’s been fascinating to gain a new understanding of how these pathways may have a role in the pathogenesis of SLE and, most importantly, it’s exciting to think about the ways in which this may ultimately translate into clinical care.

What are you working on next related to this poster? 

I will seek to identify the precise mechanism that results in impaired mitochondrial function and how iron may have a role in the traditionally held views of SLE pathogenesis. I will also be aiming to assess whether it is possible to correct impaired mitochondrial function in vitro though the addition of drugs, with the ultimate aim of potentially finding novel agents that can be translated for use in future clinical trials.