Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Science 2 December 2005:
Vol. 310. no. 5753, p. 1393
DOI: 10.1126/science.310.5753.1393a
Prev | Table of Contents | Next

Editors' Choice: Highlights of the recent literature

Pathogens have evolved countless devious means of thriving within their hosts. These range from antigenic escape from the attention of B and T cells to usurping the early detection network of the innate immune system.

Wilson et al. provide evidence to suggest that the nematode gut parasite Heligmosomoides polygyrus protects itself by suppressing allergic T cell responses in the host. Nematode infection was found to decrease the pulmonary allergic inflammation normally evoked in mice by an allergen from the house dust mite. Tying several lines of evidence together, the effects were narrowed to a population of regulatory CD4 T cells from gut-associated lymph nodes of infected mice. Smith et al. found that another helminth, the trematode parasite Schistosoma mansoni, produces a chemokine-binding protein (CKBP) to protect itself from the ill effects of host inflammation. CKBP was detected specifically in the egg stage of the parasite and bound CXCL8 (IL-8) and CCL3 (MIP1a). Predominantly through effects on neutrophil activity, CKBP inhibited different forms of experimental inflammation in mice. Both studies reveal a new layer of diversity by which helminths modify their host environment. -- SJS

J. Exp. Med. 202, 1199; 1319 (2005).




ADVERTISEMENT
Click Me!

ADVERTISEMENT
Click Me!

To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)