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The human immune response during cutaneous leishmaniasis: NO problem.
M D Mossalayi1, M Arock, D Mazier
1Hematology Laboratory, Faculty of Pharmacy Paris V, 4 Avenue de l'Observatoire, 75006 Paris, France. Djavad.Mossalayi@umr5540.u-bordeaux2.fr
Parasitology Today (Personal Ed.)
|July 17, 1999
Summary
The low-affinity IgE receptor (CD23) on macrophages may mediate nitric oxide (NO) release, contributing to host protection and disease progression in cutaneous leishmaniasis.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Increased expression of the low-affinity IgE receptor (CD23) and IgE levels occur during helminth infections, but their precise roles are unclear.
- CD23 crosslinking promotes intracellular killing of Leishmania parasites in macrophages via TNF-alpha and nitric oxide (NO) production.
Purpose of the Study:
- To propose a model for the immune response involving CD23-IgE-mediated NO release in human cutaneous leishmaniasis.
Main Methods:
- In vitro and in vivo studies of human cutaneous leishmaniasis.
Main Results:
- CD23-IgE interaction is proposed to mediate NO release.
Conclusions:
- CD23-IgE-mediated NO release plays a role in both host protection and active cutaneous leishmaniasis.