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Infection and Immunity, September 2004, p. 5331-5339, Vol. 72, No. 9
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.9.5331-5339.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Dendritic Cells Induce Immunity and Long-Lasting Protection against Blood-Stage Malaria despite an In Vitro Parasite-Induced Maturation Defect

Dodie S. Pouniotis, Owen Proudfoot, Violeta Bogdanoska,{dagger} Vasso Apostolopoulos, Theodora Fifis, and Magdalena Plebanski*

Vaccine and Infectious Diseases Unit, The Austin Research Institute, Heidelberg, Victoria, Australia

Received 23 December 2003/ Returned for modification 3 February 2004/ Accepted 16 March 2004

Dendritic cells (DC) suffer a maturation defect following interaction with erythrocytes infected with malaria parasites and become unable to induce protective malaria liver-stage immunity. Here we show that, by contrast, maturation-arrested DC in vitro are capable of the successful induction of antigen-specific gamma interferon (IFN-{gamma}) and interleukin 4 (IL-4) T-cell responses, antibody responses, and potent protection against lethal blood-stage malaria challenge in vivo. Similar results were found with DC pulsed with intact parasitized Plasmodium yoelii or Plasmodium chabaudi erythrocytes. Cross-strain protection was also induced. High levels of protection (80 to 100%) against lethal challenge were evident from 10 days after a single immunization and maintained up to 120 days. Interestingly, correlation studies versus blood-stage protection at different time points suggest that the immune effector mechanisms associated with protection could change over time. Antibody-independent, T-cell- and IL-12-associated protection was observed early after immunization, followed by antibody and IL-4-associated, IFN-{gamma}-independent protection in long-term studies. These results indicate that DC, even when clearly susceptible to parasite-induced maturation defect effects in vitro, can be central to the induction of protection against blood-stage malaria in vivo.

* Corresponding author. Mailing address: Vaccine and Infectious Diseases Unit, The Austin Research Institute, Austin Campus Heidelberg, Victoria 3084, Australia. Phone: 61 3 92870673. Fax: 61 3 92870600. E-mail: mplebans{at}ari.unimelb.edu.au.

Editor: W. A. Petri, Jr.

{dagger} Present address: CRC for Chronic Inflammatory Diseases, The University of Melbourne, Department of Medicine, Royal Melbourne Hospital, Parkville, Victoria 3050, Austrailia.

Infection and Immunity, September 2004, p. 5331-5339, Vol. 72, No. 9
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.9.5331-5339.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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