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Seropositive Human Subjects Produce Interferon Gamma after Stimulation with Recombinant Cryptosporidium hominis gp15

Cryptosporidiosis is an important cause of diarrhea worldwide. In normal hosts, infection is self-limited and associated with seroconversion and partial immunity to reinfection. Immunity is associated with interferon gamma (IFN) production. Cryptosporidium surface proteins gp15 and gp40 are among the immunodominant proteins in terms of antibody responses. We asked the question of whether these antigens also stimulate production of IFN in patients who have serologic evidence of prior infection. Whole blood from seropositive donors was stimulated with recombinant gp15 and gp 40 from Cryptosporidium hominis and Cryptosporidium parvum or His-tag controls. C. hominis gp15 stimulated increased production of IFN. By contrast, there was no significant increase after stimulation with C. parvum gp15 or either gp40 preparation. IFN production in response to C. hominis gp15 was noted in both CD4⁺ and CD8⁺ cells. This highlights the potential for C. hominis gp15 as a vaccine candidate for human cryptosporidiosis.

Received March 1, 2007. Accepted for publication May 18, 2007.

Acknowledgments: The authors thank Anne Kane of the GRASP Digestive Diseases Center and Geneve Allison of the Tufts–New England Medical Center for preparation of the recombinant antigen. The protocol and consent forms were approved by the Institutional Review Board of Baylor College of Medicine.

Financial support: This work was supported by the National Institutes of Health (grants R01 AI041735 to A.C.W. and R01 AI07389 to H.D.W.), the Baylor UT Houston Center for AIDS Research (P30 AI36211), the Texas Gulf Coast Digestive Diseases Center (P30 DK056338), the GRASP Digestive Diseases Center (P30 DK34928) at Tufts–New England Medical Center, and a training grant (T32 AI07389 to K.R.).

^* Address correspondence to A. Clinton White Jr., Infectious Disease Division, Department of Internal Medicine, University of Texas Medical Branch, 301 University Boulevard, Route 0435 Galveston, TX 77555. E-mail: acwhite{at}utmb.edu

Authors’ addresses: Geoffrey A. Preidis, Translational Biology and Molecular Medicine Program, Infectious Disease Section Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Dorothy E. Lewis, Department of Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Edward A. Gravis, Department of Pathology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. H.C. Wang, USAMRD-WRAIR, Brooks City Base, TX. K.A. Rogers, Cell Signaling Technology, Inc., Danvers, MA 01923. Honorine D. Ward, Tufts-New England Medical Center, Division of Geographic Medicine and Infectious Diseases, 750 Washington Street, Boston, MA 02111. A. Castellanos-Gonzalez and A.C. White, Infectious Disease Division, Department of Internal Medicine, University of Texas Medical Branch, 301 University Boulevard, Route 0435 Galveston, TX 77555, Telephone: +1 (409) 747-0234, Fax: +1 (409) 772-6527, E-mail: acwhite{at}utmb.edu.