CD4+ T cells mediate mucosal and systemic immune responses to experimental hookworm infection
Document Type
Article
Department or Administrative Unit
Biological Sciences
Publication Date
6-2010
Abstract
Hookworm infection is associated with anaemia and malnutrition in many resource-limited countries. Ancylostoma hookworms have previously been shown to modulate host cellular immune responses through multiple mechanisms, including reduced mitogen-mediated lymphocyte proliferation, impaired antigen presentation/processing, and relative reductions in CD4+ T cells in the spleen and mesenteric lymph nodes. Syrian hamsters were depleted of CD4+ for up to 9 days following intraperitoneal injection (200 μg) of a murine anti-mouse CD4 monoclonal IgG (clone GK1·5). CD4+ T-cell-depleted hamsters infected with the hookworm Ancylostoma ceylanicum exhibited a threefold higher mean intestinal worm burden and more severe anaemia than animals that received isotype control IgG. In addition, depletion of CD4+ T cells was associated with impaired cellular and humoral (serum and mucosal) immune responses to hookworm antigens. These data demonstrate an effector role for CD4+ T cells in hookworm immunity and disease pathogenesis. Ultimately, these studies may yield important insights into the relationship between intestinal nematode infections and diseases that are associated with CD4+ T-cell depletion, including HIV.
Recommended Citation
Dondji, B., Sun, T., Bungiro, R. D., Vermeire, J. J., Harrison, L. M., Bifulco, C., & Cappello, M. (2010). CD4+ T cells mediate mucosal and systemic immune responses to experimental hookworm infection. Parasite Immunology, 32(6), 406–413. https://doi.org/10.1111/j.1365-3024.2010.01204.x
Journal
Parasite Immunology
Copyright
© 2010 Blackwell Publishing Ltd
Comments
This article was originally published in Parasite Immunology. The full-text article from the publisher can be found here.
An author's accepted manuscript version is available on PubMed Central.
Due to copyright restrictions, this article is not available for free download from ScholarWorks @ CWU.