NDLI: Separable functions of Nef disrupt two aspects of T cell receptor machinery: CD4 expression and CD3 signaling.

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Separable functions of Nef disrupt two aspects of T cell receptor machinery: CD4 expression and CD3 signaling.

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Separable functions of Nef disrupt two aspects of T cell receptor machinery: CD4 expression and CD3 signaling.

Content Provider	PubMed Central
Author	Iafrate, A. J. Bronson, S. Skowronski, J.
Abstract	The Nef protein alters T cell receptor (TCR) signaling in T cells and is critical for the pathogenesis of AIDS. We used a transient expression assay in a human CD4+ T cell line to analyze the interaction of Nef with the TCR machinery. We show that, in addition to down-regulating CD4 expression on the cell surface, Nef blocks a receptor-proximal event in CD3 signaling. Analysis of a large number of mutant Nef proteins demonstrated that the effects of Nef on CD4 expression and on CD3 signaling are separable. The ability of Nef to block CD3 signaling was selectively abolished by mutations in the central part of the Nef protein and in particular by those known to disrupt the SH3 binding surface in the structured core of Nef. In contrast, the ability of Nef to down-regulate CD4 expression was selectively abolished by two clusters of mutations, one in the N-terminal and one in the C-terminal region of Nef. These two regions correspond to the two flexible loops in Nef as predicted by solution NMR analysis. We show that this general functional organization is conserved between the Nef proteins of the human and simian immunodeficiency viruses (HIV-1 and SIV). Our data demonstrate that Nef has at least two independent mechanisms to alter TCR function and thus may interfere with a range of T cell responses.
Related Links	http://dx.doi.org/10.1093/emboj/16.4.673
Starting Page	673
File Format	PDF
ISSN	14602075
e-ISSN	14602075
Journal	The EMBO Journal
Issue Number	4
Volume Number	16
Language	English
Publisher Date	1997-02-17
Access Restriction	Open
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Microbiology Medicine Molecular Biology

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