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Infection and Immunity, March 2006, p. 1547-1554, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1547-1554.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Antigen-Responsive CD4⁺ T Cells from C3H Mice Chronically Infected with Leishmania amazonensis Are Impaired in the Transition to an Effector Phenotype

Amanda E. Ramer,^1,2 Yannick F. Vanloubbeeck,^2, and Douglas E. Jones^1,2*

Immunobiology Program,¹ Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, Iowa 50011-1250²

Received 28 October 2005/ Returned for modification 7 December 2005/ Accepted 21 December 2005

C3HeB/FeJ mice challenged with Leishmania major develop a polarized Th1 response and subsequently heal, whereas Leishmania amazonensis challenge leads to chronic lesions with high parasite loads at 10 weeks postinfection. In this study, a comparison of draining lymph node cells from L. amazonensis- and L. major-infected mice at 10 weeks postinfection showed equivalent percentages of effector/memory phenotype CD44^hi CD4⁺ T cells producing interleukin-2 (IL-2) and proliferating after antigen stimulation. However, these cells isolated from L. amazonensis-infected mice were not skewed toward either a Th1 or Th2 phenotype in vivo, as evidenced by their unbiased Th1/Th2 transcription factor mRNA profile. In vivo antigen stimulation with added IL-12 failed to enhance gamma interferon (IFN-) production of CD4⁺ T cells from L. amazonensis-infected mice. Antigen stimulation of CD4⁺ T cells from L. amazonensis-infected mice in vitro in the presence of IL-12 resulted in production of only 10 to 15% of the IFN- produced by T cells from L. major-infected mice under identical conditions. These results suggest that the CD4⁺ T-cell response during chronic L. amazonensis infection is limited during the transition from an early activated CD4⁺ T-cell population to an effector cell population and demonstrate that these T cells have an intrinsic defect beyond the presence or absence of IL-12 during antigen stimulation.

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* Corresponding author. Mailing address: Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, IA 50011-1250. Phone: (515) 294-3282. Fax: (515) 294-5423. E-mail: jonesdou{at}iastate.edu.

Editor: W. A. Petri, Jr.

Present address: Department of Medicine, Division of Hematology/Oncology, University of California—San Francisco, San Francisco, CA 94143.

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Infection and Immunity, March 2006, p. 1547-1554, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1547-1554.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

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