This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zhao, Y.
Right arrow Articles by Yap, G. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhao, Y.
Right arrow Articles by Yap, G. S.

 Previous Article  |  Next Article 

Infection and Immunity, October 2007, p. 4799-4803, Vol. 75, No. 10
0019-9567/07/$08.00+0     doi:10.1128/IAI.00738-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Rapid Elimination of Toxoplasma gondii by Gamma Interferon-Primed Mouse Macrophages Is Independent of CD40 Signaling{triangledown}

Yanlin Zhao, Douglas Wilson, Suzanne Matthews, and George S. Yap*

Department of Molecular Microbiology and Immunology, Warren Alpert Medical School, Brown University, Providence, Rhode Island 02912

Received 31 May 2007/ Returned for modification 30 June 2007/ Accepted 24 July 2007

Autophagy has been implicated in the intracellular destruction of Toxoplasma gondii by primed macrophages following gamma interferon (IFN-{gamma}) activation of p47 GTPases. CD40 ligation has also been shown to trigger autophagic elimination of T. gondii independent of IFN-{gamma} and p47 GTPases. Here we demonstrate that IFN-{gamma}/p47 GTPase-dependent elimination of T. gondii by strain CPS vaccine-primed macrophages is independent of CD40/tumor necrosis factor signaling. Similar to wild-type controls, both CD40-deficient and tumor necrosis factor receptor 1/2 (TNFR1/2)-deficient macrophages can efficiently eliminate invaded strain GFP-PTG and restrain its replication following priming. In contrast, macrophages from mice lacking the IFN-{gamma} receptor gene neither clear the parasites nor repress their proliferation. Thus, CD40 and IFN-{gamma}-induced pathogen elimination might represent two independent resistance pathways, the latter of which plays a primary role in anti-Toxoplasma immunity in mice.

* Corresponding author. Mailing address: Box G-B6, Department of Molecular Microbiology and Immunology, Warren Alpert Medical School, Brown University, Providence, RI 02912. Phone: (401) 863-3483. Fax: (401) 863-1971. E-mail: george_yap{at}brown.edu

{triangledown} Published ahead of print on 6 August 2007.

Editor: W. A. Petri, Jr.

Infection and Immunity, October 2007, p. 4799-4803, Vol. 75, No. 10
0019-9567/07/$08.00+0     doi:10.1128/IAI.00738-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Zhao, Y., Ferguson, D. J. P., Wilson, D. C., Howard, J. C., Sibley, L. D., Yap, G. S. (2009). Virulent Toxoplasma gondii Evade Immunity-Related GTPase-Mediated Parasite Vacuole Disruption within Primed Macrophages. J. Immunol. 182: 3775-3781 [Abstract] [Full Text]  
  • Goldszmid, R. S., Coppens, I., Lev, A., Caspar, P., Mellman, I., Sher, A. (2009). Host ER-parasitophorous vacuole interaction provides a route of entry for antigen cross-presentation in Toxoplasma gondii-infected dendritic cells. JEM 206: 399-410 [Abstract] [Full Text]  
  • Gigley, J. P., Fox, B. A., Bzik, D. J. (2009). Cell-Mediated Immunity to Toxoplasma gondii Develops Primarily by Local Th1 Host Immune Responses in the Absence of Parasite Replication. J. Immunol. 182: 1069-1078 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»