PARASITIC worms could have an unexpected benefit: they could improve the prospects of people with autoimmune diseases such as multiple sclerosis (MS).
Parasites are already known to affect the progression of such diseases in animals, so Jorge Correale and Mauricio Farez at the Ra煤l Carrea Institute for Neurological Research in Buenos Aires, Argentina, wanted to know if they did the same in people. They followed the progression of MS in 24 people, half of whom were recently diagnosed with parasitic infection. For nearly five years, the subjects were checked regularly for any worsening of symptoms, and during the final 18 months of the study their blood was examined for immune cell activity.
Sure enough, those infected with parasites had fewer relapses and less deterioration in their condition than the parasite-free participants, the pair found. Overall, there were just three relapses in the parasite group compared with 56 in the uninfected group (Annals of Neurology, DOI: 10.1002/ana.21067). 鈥淭his is the first direct evidence that parasites might be relevant to protection from an autoimmune disease,鈥� says Graham Rook, an immunologist at University College London.
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鈥淢S patients with parasitic infections had fewer relapses than those patients who were parasite-free鈥�
The findings echo the observation in Vietnam that children infected with parasites had fewer allergies than uninfected children (New Scientist, 6 January, p 15). They also support a revised version of the so-called 鈥渉ygiene hypothesis鈥�, which suggests that allergies have become more common in recent decades because we are exposed to fewer infections as children.
Bacterial and viral infections trigger a subset of immune cells called TH1 cells, while a different subset called TH2 cells deal with allergies. The assumption was that in developed countries, where micro-organisms are thought to be less prevalent thanks to higher standards of hygiene, the balance tips towards TH2 cells, and so people develop more allergies.
What this simple version of the hygiene hypothesis cannot explain is why the incidence of autoimmune diseases, which are mediated by TH1 cells, has also risen steadily in developed countries. The answer, Correale and Farez suggest, may lie with a different set of immune cells called regulatory T (Treg) cells, which control both TH1 and TH2 responses. In their study, the pair showed that patients with parasitic worms and MS had more Treg cells than people with MS who did not have worms.
Rook has now updated the hygiene hypothesis to take such observations into account. Certain bacteria and parasites have lived with humans for millennia and have evolved ways of stimulating Treg cells to dampen down the immune system, allowing the parasites to survive in the body. Modern standards of hygiene mean that these 鈥渙ld friends鈥� are now gone, so Treg cells have become less active. This in turn may have allowed the TH1 and TH2 cells to go into overdrive, triggering allergies and autoimmune diseases.
Some experimental drugs are designed to interfere with Treg cell activity (New Scientist, 23 March 2006, p 10), and Correale and Farez鈥檚 work suggests that parasites might provide an alternative mechanism for dampening down immune responses. However, Correale cautions that parasites may also induce different regulatory mechanisms. 鈥淎 better knowledge of the immune response during autoimmunity and parasite infection will allow us to select the best strategy for treatment,鈥� he says.
