Seminar Series on Evolutionary Medicine - Andrea Graham: Why do immune systems harm their bearers? - The evolutionary biology of "friendly fire"
- Date: Jan 25, 2018
- Time: 03:00 PM - 04:00 PM (Local Time Germany)
- Speaker: Andrea Graham from Princeton University, USA
- Please find more information on the speaker here: http://algraham.princeton.edu/
- Location: MPI Plön
- Room: Lecture hall
- Host: Tobias Lenz and John Baines
Abstract
Immune-mediated diseases ranging from septic shock to multiple sclerosis
exact a huge toll on human health. Many of the molecular and cellular
mechanisms by which the immune system can harm a host’s own tissues or
even cause death are well understood. However, evolutionary
explanations for self-harm have received less attention. What forces of
natural selection have generated such a remarkable immune system –
capable of feats like memory responses that protect against particular
influenza strains decades after first exposure – that also is capable of
causing such tremendous damage to our own bodies? I will tackle that
question, presenting an emerging understanding of the evolutionary
causes of immune-mediated disease, including important roles for
susceptibility trade-offs and for long-term co-evolution with parasites
such as gastrointestinal worms. For example, in wild sheep,
autoimmunity is associated with enhanced resistance to infectious
diseases. Hosts may thus experience a trade-off: a host could be
susceptible to autoimmune diseases OR infections, but not both. Such a
trade-off could help to explain the persistence of diseases like lupus.
Recent tests suggest that this trade-off is borne out in human
populations. Furthermore, the clearance of our co-evolved
gastrointestinal worms can alter immune system balance in a way that
exacerbates autoimmune disease. Will the future of medicine entail
“restoration ecology” of the human gut, reinstating worms to rein in
diseases like ulcerative colitis? Heterogeneity in susceptibility to
autoimmune diseases demands evolutionary explanation and arguably will
shed light on heterogeneity in human infectious disease susceptibility.