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Infection and Immunity, March 2001, p. 1630-1634, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1630-1634.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Marrow-Derived CD40-Positive Cells Are Required for Mice To Clear Cryptosporidium parvum Infection

Anthony R. Hayward,* Mary Cosyns, Michelle Jones, and Esther M. Ponnuraj

Departments of Pediatrics and Immunology and the Barbara Davis Childhood Diabetes Center, University of Colorado School of Medicine, Denver, Colorado

Received 5 September 2000/Returned for modification 11 October 2000/Accepted 12 December 2000

To clear a Cryptosporidium parvum infection, mice need CD4+ T cells, major histocompatibility complex class II, and an intact CD40-CD154 signaling pathway. CD40 is constitutively expressed on marrow-derived cells such as dendritic cells and B lymphocytes and is induced by gamma interferon (IFN-gamma ) on most somatic cells. To determine whether the CD40 needed to clear a C. parvum infection has to be on marrow-derived mononuclear cells or on the epithelial cells that normally harbor the parasite, we transplanted CD40-/- mice with CD40+/- bone marrow and then infected them with C. parvum. These chimeras cleared the C. parvum infection, while CD40+/- controls transplanted with CD40-/- marrow cells remained infected. CD40 expression on marrow-derived cells therefore suffices for a C. parvum infection to be cleared, while CD40 expression on intestinal epithelial cells is not sufficient. There was no difference between the acquisition of CD69 and CD154 by mesenteric lymph node T cells of C. parvum-infected animals with intact or disrupted CD40-CD154 pathways. CD4 T cells entered the intestinal laminae propriae of C. parvum-infected animals whether or not the CD40 genes of these recipients were intact. These results suggest that, for a C. parvum infection to be cleared, CD40 is not necessary for T-cell activation but may instead contribute to an effector pathway of marrow-derived cells.

* Corresponding author. Mailing address: B 140, UCHSC, Denver, CO 80262. Phone: (303) 315-7462. Fax: (303) 315-4892. E-mail: anthony.hayward{at}uchsc.edu.

Infection and Immunity, March 2001, p. 1630-1634, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1630-1634.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Takeuchi, D., Jones, V. C., Kobayashi, M., Suzuki, F. (2008). Cooperative Role of Macrophages and Neutrophils in Host Antiprotozoan Resistance in Mice Acutely Infected with Cryptosporidium parvum. Infect. Immun. 76: 3657-3663 [Abstract] [Full Text]  
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  • Morales, M. A. G., Mele, R., Ludovisi, A., Bruschi, F., Tosini, F., Pozio, E. (2004). Cryptosporidium parvum-Specific CD4 Th1 Cells from Sensitized Donors Responding to Both Fractionated and Recombinant Antigenic Proteins. Infect. Immun. 72: 1306-1310 [Abstract] [Full Text]  
  • Ponnuraj, E. M., Hayward, A. R. (2001). Intact Intestinal mRNAs and Intestinal Epithelial Cell Esterase, But Not Cryptosporidium parvum, Reach Mesenteric Lymph Nodes of Infected Mice. J. Immunol. 167: 5321-5328 [Abstract] [Full Text]  


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