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Immune responses in trachoma, and more

Trachoma, which is caused by ocular infection with Chlamydia trachomatis, remains the leading infectious cause of blindness and in 2002 was responsible for 3.6% of total global blindness. In a paper published in PLoS Medicine, Martin Holland and colleagues from the London School of Hygiene and Tropical Medicine have studied the human immune response to this infection in a population where trachoma is very common.

The researchers studied 345 children in the Gambia, who could be divided into four groups based on infection with C. trachomatis and clinical signs. Some children--particularly the older ones--were uninfected and had no clinical signs. Others were infected but showed no clinical signs--these children were incubating the bacteria. Some were infected and had clinical disease; these children had the highest bacterial loads. Finally, children recovering from an infection carried no bacteria but still had some clinical signs. The researchers detected different types of immune response in each of these groups.

Children incubating the bacteria had a strong pro-inflammatory response--their immune systems were trying to fight off infection. The pro-inflammatory response was even stronger in the infected children with clinical signs, but the regulatory response was also increased, presumably to limit inflammation. In children in the recovery phase, only regulatory immune cells, which were making mRNA from a gene called FOXP3, remained active.

These results suggest that the interaction between the infection and the clinical disease process is complex and that regulatory immune cells are important in limiting the inflammatory response to this infection. This information about immune responses at different stages of infection with C. trachomatis may help in the design of vaccines to prevent this infection.

Citation: Faal N, Bailey RL, Jeffries D, Joof H, Sarr I, et al. (2006) Conjunctival FOXP3 expression in trachoma: Do re
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Contact: Andrew Hyde
press@plos.org
44-122-346-3330
Public Library of Science
7-Aug-2006


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