Abstract：
:The Nef protein of HIV-1 mediates immune evasion by relocating major histocompatibility complex (MHC) molecules and the immune costimulatory molecules CD80 and CD86 away from the monocytic cell surface. We describe a two-pronged mechanism by which Nef removes CD80 and CD86 from the cell surface. While MHCI, CD80, and CD86 are all internalized via a dynamin-independent pathway, the endocytic mechanism used for costimulatory molecules is distinct from MHCI relocation. Nef expression results in the activation and actin-dependent translocation of Src kinase to the cell periphery. At the cell surface, Src promotes Rac activation via TIAM, a guanine nucleotide exchange factor for Rac. Nef also binds to the cytosolic tails of CD80 and CD86, triggering their endocytosis via Rac-based actin polymerization. These data reveal the use of an unusual molecular mechanism triggered in the host cell by HIV to affect its viral immune evasion strategy and suggest approaches for its subversion.
journal_name
Cell Host Microbejournal_title
Cell host & microbeauthors
Chaudhry A,Das SR,Jameel S,George A,Bal V,Mayor S,Rath Sdoi
10.1016/j.chom.2007.01.001subject
Has Abstractpub_date
2007-03-15 00:00:00pages
37-49issue
1eissn
1931-3128issn
1934-6069pii
S1931-3128(07)00003-0journal_volume
1pub_type
杂志文章abstract：:To maintain tissue homeostasis and avoid disease, epithelial cells damaged by pathogens need to be readily replenished, and this is mainly achieved by the activation of stem cells. In this Short Review, we discuss recent developments in the exciting field of host epithelia-pathogen interaction in Drosophila as well as...
journal_title：Cell host & microbe
pub_type： 杂志文章,评审
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abstract：:The Salmonella enterica effector SteD depletes mature MHC class II (mMHCII) molecules from the surface of infected antigen-presenting cells through ubiquitination of the cytoplasmic tail of the mMHCII β chain. Here, through a genome-wide mutant screen of human antigen-presenting cells, we show that the NEDD4 family HE...
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journal_title：Cell host & microbe
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journal_title：Cell host & microbe
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journal_title：Cell host & microbe
pub_type： 评论,杂志文章
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journal_title：Cell host & microbe
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journal_title：Cell host & microbe
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journal_title：Cell host & microbe
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journal_title：Cell host & microbe
pub_type： 评论,杂志文章
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journal_title：Cell host & microbe
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journal_title：Cell host & microbe
pub_type： 评论,杂志文章
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journal_title：Cell host & microbe
pub_type： 杂志文章
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journal_title：Cell host & microbe
pub_type： 评论,杂志文章
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journal_title：Cell host & microbe
pub_type： 杂志文章,评审
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journal_title：Cell host & microbe
pub_type： 杂志文章,评审
doi：10.1016/j.chom.2014.10.008
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journal_title：Cell host & microbe
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journal_title：Cell host & microbe
pub_type： 杂志文章
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journal_title：Cell host & microbe
pub_type： 评论,杂志文章
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journal_title：Cell host & microbe
pub_type： 评论,杂志文章
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journal_title：Cell host & microbe
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journal_title：Cell host & microbe
pub_type： 评论,杂志文章
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journal_title：Cell host & microbe
pub_type： 评论,杂志文章
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journal_title：Cell host & microbe
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journal_title：Cell host & microbe
pub_type： 杂志文章
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journal_title：Cell host & microbe
pub_type： 杂志文章
doi：10.1016/j.chom.2015.12.011
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abstract：:RNA interference (RNAi) has been extensively used to identify host factors affecting virus infection but requires exogenous delivery of short interfering RNAs (siRNAs), thus limiting the technique to nonphysiological infection models and a single defined cell type. We report an alternative screening approach using siR...
journal_title：Cell host & microbe
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