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dc.contributor.authorLittwitz-Salomon, Elisabeth
dc.contributor.authorAkhmetzyanova, Ilseyar
dc.contributor.authorVallet, Cecilia
dc.contributor.authorFrancois, Sandra
dc.contributor.authorDittmer, Ulf
dc.contributor.authorGibbert, Kathrin
dc.date.accessioned2015-09-01T17:59:46Z
dc.date.available2015-09-01T17:59:46Z
dc.date.issued2015-07-30
dc.identifier.citationRetrovirology. 2015 Jul 30;12(1):66
dc.identifier.urihttp://dx.doi.org/10.1186/s12977-015-0191-3
dc.identifier.urihttp://hdl.handle.net/10724/31923
dc.description.abstractAbstract Background It is well established that effector T cell responses are crucial for the control of most virus infections, but they are often tightly controlled by regulatory T cells (Treg) to minimize immunopathology. NK cells also contribute to virus control but it is not known if their antiviral effect is influenced by virus-induced Tregs as well. We therefore analyzed whether antiretroviral NK cell functions are inhibited by Tregs during an acute Friend retrovirus infection of mice. Results Selective depletion of Tregs by using the transgenic DEREG mouse model resulted in improved NK cell proliferation, maturation and effector cell differentiation. Suppression of NK cell functions depended on IL-2 consumption by Tregs, which could be overcome by specific NK cell stimulation with an IL-2/anti-IL-2 mAb complex. Conclusions The current study demonstrates that virus-induced Tregs indeed inhibit antiviral NK cell responses and describes a targeted immunotherapy that can abrogate the suppression of NK cells by Tregs.
dc.titleActivated regulatory T cells suppress effector NK cell responses by an IL-2-mediated mechanism during an acute retroviral infection
dc.typeJournal Article
dc.date.updated2015-07-29T19:08:18Z
dc.language.rfc3066en
dc.rights.holderLittwitz-Salomon et al.


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