Early Enhanced Th1 Response after Leishmania amazonensis Infection of C57BL/6 Interleukin-10-Deficient Mice Does Not Lead to Resolution of Infection

dc.contributor.author Jones, Douglas
dc.contributor.author Ackermann, Mark
dc.contributor.author Ackermann, Mark
dc.contributor.author Wille, Ulrike
dc.contributor.author Hunter, Christopher
dc.contributor.author Scott, Phillip
dc.contributor.department Veterinary Pathology
dc.date 2018-02-13T06:20:27.000
dc.date.accessioned 2020-07-07T05:15:45Z
dc.date.available 2020-07-07T05:15:45Z
dc.date.copyright Tue Jan 01 00:00:00 UTC 2002
dc.date.embargo 2013-02-25
dc.date.issued 2002-04-01
dc.description.abstract <p>C3H and C57BL/6 mice are resistant to <em>Leishmania major</em> but develop chronic lesions with persistent parasite loads when they are infected with <em>Leishmania amazonensis</em>. 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 <em>L. amazonensis</em> 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 <em>L. amazonensis</em>resistance 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.</p>
dc.description.comments <p>This article is from <em>Infection and Immunity </em>70, no. 4 (April 2002): 2151–2158, doi:<a href="http://dx.doi.org/10.1128/IAI.70.4.2151-2158.2002" target="_blank">10.1128/IAI.70.4.2151-2158.2002</a>.</p>
dc.format.mimetype application/pdf
dc.identifier archive/lib.dr.iastate.edu/vpath_pubs/15/
dc.identifier.articleid 1013
dc.identifier.contextkey 3783957
dc.identifier.s3bucket isulib-bepress-aws-west
dc.identifier.submissionpath vpath_pubs/15
dc.identifier.uri https://dr.lib.iastate.edu/handle/20.500.12876/92437
dc.language.iso en
dc.source.bitstream archive/lib.dr.iastate.edu/vpath_pubs/15/2002_Jones_EarlyEnhancedTh1.pdf|||Fri Jan 14 20:30:21 UTC 2022
dc.source.uri 10.1128/​IAI.70.4.2151-2158.2002
dc.subject.disciplines Veterinary Pathology and Pathobiology
dc.title Early Enhanced Th1 Response after Leishmania amazonensis Infection of C57BL/6 Interleukin-10-Deficient Mice Does Not Lead to Resolution of Infection
dc.type article
dc.type.genre article
dspace.entity.type Publication
relation.isAuthorOfPublication 86c1ed73-b60d-48ce-8f35-449bc320a693
relation.isOrgUnitOfPublication cf38d7e3-b5f8-4859-83e3-ae8fab6a4c5f
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