Skip to main content
Article
Early Enhanced Th1 Response after Leishmania amazonensis Infection of C57BL/6 Interleukin-10-Deficient Mice Does Not Lead to Resolution of Infection
Infection and Immunity
  • Douglas E. Jones, Iowa State University
  • Mark R. Ackermann, Iowa State University
  • Ulrike Wille, University of Pennsylvania
  • Christopher A. Hunter, University of Pennsylvania
  • Phillip Scott, University of Pennsylvania
Document Type
Article
Publication Date
4-1-2002
DOI
10.1128/​IAI.70.4.2151-2158.2002
Abstract
C3H and C57BL/6 mice are resistant to Leishmania major but develop chronic lesions with persistent parasite loads when they are infected with Leishmania amazonensis. These lesions develop in the absence of interleukin-4 (IL-4), indicating that susceptibility to this parasite is not a result of development of a Th2 response. Expression of the cytokine IL-10 during infection could account for the lack of IL-12 expression and poor cell-mediated immunity towards the parasite. Therefore, we tested the hypothesis that IL-10 plays a central role in downmodulating the Th1 response after L. amazonensis infection. Infection of C57BL/6 IL-10-deficient mice indicated that in the absence of IL-10 there was early enhancement of a Th1 response, which was downregulated during the more chronic stage of infection. In addition, although there were 1- to 2-log reductions in the parasite loads within the lesions, the parasites continued to persist, and they were associated with chronic lesions whose size was similar to that of the control lesions. These experiments indicated that L. amazonensisresistance to killing in vivo is only partially dependent on expression of host IL-10. However, IL-10-deficient mice had an enhanced delayed-type hypersensitivity response during the chronic phase of infection, indicating that there were Th1 type effector cells in vivo at this late stage of infection. These results indicate that although IL-10 plays a role in limiting the Th1 response during the acute infection phase, other immunomodulatory factors are responsible for limiting the Th1 response during the chronic phase.
Comments

This article is from Infection and Immunity 70, no. 4 (April 2002): 2151–2158, doi:10.1128/IAI.70.4.2151-2158.2002.

Copyright Owner
American Society for Microbiology
Language
en
Date Available
February 25, 2013
File Format
application/pdf
Citation Information
Douglas E. Jones, Mark R. Ackermann, Ulrike Wille, Christopher A. Hunter, et al.. "Early Enhanced Th1 Response after Leishmania amazonensis Infection of C57BL/6 Interleukin-10-Deficient Mice Does Not Lead to Resolution of Infection" Infection and Immunity Vol. 70 Iss. 4 (2002) p. 2151 - 2158
Available at: http://works.bepress.com/mark_ackermann/24/