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Infection and Immunity, December 2005, p. 8425-8428, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8425-8428.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

An Early Intestinal Mucosal Source of Gamma Interferon Is Associated with Resistance to and Control of Cryptosporidium parvum Infection in Mice

Brett A. Leav,1* Masaru Yoshida,2 Kathleen Rogers,1 Seth Cohen,1 Nihal Godiwala,1 Richard S. Blumberg,2 and Honorine Ward1

Division of Geographic Medicine and Infectious Diseases, Tufts-New England Medical Center, Boston, Massachusetts,1 Division of Gastroenterology, Brigham and Women's Hospital, Boston, Massachusetts2

Received 18 February 2005/ Returned for modification 29 March 2005/ Accepted 2 September 2005

Resistance to and control of Cryptosporidium parvum infection in mice in the absence of adaptive immunity appears to be gamma interferon (IFN-{gamma}) dependent. Using an IFN-{gamma}-neutralizing antibody in a murine model, we demonstrated increased susceptibility to infection within 24 h. We correlated this early resistance and control with increased mucosal expression of IFN-{gamma} and demonstrate that CD8+ T-cell receptor {alpha}ß intestinal intraepithelial lymphocytes express and secrete this cytokine shortly after infection. The rapid kinetics of IFN-{gamma} expression and secretion by naive CD8+ T cells in response to a protozoan pathogen have not previously been demonstrated.


* Corresponding author. Mailing address: Division of Geographic Medicine and Infectious Diseases, Tufts-New England Medical Center, Box 041, 750 Washington Street, Boston, MA 02111. Phone: (617) 636-2869. Fax: (617) 636-5292. E-mail: bleav{at}tufts-nemc.org.

Editor: W. A. Petri, Jr.


Infection and Immunity, December 2005, p. 8425-8428, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8425-8428.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




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