Document Type
Article
Publication Date
4-1999
Publication Title
Infection and Immunity
Department
Geisel School of Medicine
Abstract
Microsporidia are obligate intracellular protozoan parasites that cause a wide variety of opportunistic infection in patients with AIDS. Because it is able to grow in vitro, Encephalitozoon cuniculi is currently the best-studied microsporidian. T cells mediate protective immunity against this parasite. Splenocytes obtained from infected mice proliferate in vitro in response to irradiated parasites. A transient state of hyporesponsiveness to parasite antigen and mitogen was observed at day 17 postinfection. This downregulatory response could be partially reversed by addition of nitric oxide (NO) antagonist to the culture. Mice infected withE. cuniculi secrete significant levels of gamma interferon (IFN-γ). Treatment with antibody to IFN-γ or interleukin-2 (IL-12) was able to neutralize the resistance to the parasite. Mutant animals lacking the IFN-γ or IL-12 gene were highly susceptible to infection. However, mice unable to secrete NO withstood high doses of parasite challenge, similar to normal wild-type animals. These studies describe an IFN-γ-mediated protection against E. cuniculi infection that is independent of NO production.
Original Citation
Khan IA, Moretto M. Role of gamma interferon in cellular immune response against murine Encephalitozoon cuniculi infection. Infect Immun. 1999;67(4):1887-1893.
Dartmouth Digital Commons Citation
Khan, Imtiaz A. and Moretto, Magali, "Role of Gamma Interferon in Cellular Immune Response against Murine Encephalitozoon cuniculi Infection" (1999). Dartmouth Scholarship. 984.
https://digitalcommons.dartmouth.edu/facoa/984
Included in
Infectious Disease Commons, Medical Immunology Commons, Medical Microbiology Commons, Parasitic Diseases Commons