Linked Life Data

21108466

Source:http://linkedlifedata.com/resource/pubmed/id/21108466

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pubmed-article:21108466pubmed:dateCreated2010-11-25lld:pubmed
pubmed-article:21108466pubmed:abstractTextImmunoproteasomes containing the IFN-inducible subunits ?1i (LMP2), ?2i (MECL-1) and ?5i (LMP7) alter proteasomal cleavage preference and optimize the generation of peptide ligands of MHC class I molecules. Here, we report on an unexpected new function of immunoproteasome subunits for the survival and expansion of CD4(+) and CD8(+) T cells during viral infection of mice. The effect of immunoproteasome subunit deficiency on T-cell survival upon adoptive transfer was most prominent for the lack of LMP7 followed by MECL-1 and LMP2. The survival of T cells in uninfected mice or the homeostatic expansion after transfer into RAG-2(-/-) mice was not affected by the lack of the immunosubunits. Lymphocytic choriomeningitis virus (LCMV)-specific CD8(+) T cells lacking LMP7 or MECL-1 started to divide after transfer into LCMV-infected mice but experienced a considerable cell loss within 2 days after transfer. We provide strong evidence that the loss of immunoproteasome-deficient T cells after transfer is not a consequence of graft rejection by the host, but instead is based on the requirement for immunoproteasomes for the survival of T cells in LCMV-infected mice. Therefore, the immunoproteasome may qualify as a potential new target for the suppression of undesired proinflammatory T-cell responses.lld:pubmed
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pubmed-article:21108466pubmed:authorpubmed-author:BaslerMichael...lld:pubmed
pubmed-article:21108466pubmed:authorpubmed-author:MoebiusJacque...lld:pubmed
pubmed-article:21108466pubmed:copyrightInfoCopyright © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.lld:pubmed
pubmed-article:21108466pubmed:issnTypeElectroniclld:pubmed
pubmed-article:21108466pubmed:volume40lld:pubmed
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pubmed-article:21108466pubmed:year2010lld:pubmed
pubmed-article:21108466pubmed:articleTitleImmunoproteasomes are essential for survival and expansion of T cells in virus-infected mice.lld:pubmed
pubmed-article:21108466pubmed:affiliationDivision of Immunology, Department of Biology, Constance University, Konstanz, Germany.lld:pubmed
pubmed-article:21108466pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21108466pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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