NDLI: Viral induction of AID is independent of the interferon and the Toll-like receptor signaling pathways but requires NF-κB

Content Provider	PubMed Central
Author	Gourzi, Polyxeni Leonova, Tatyana Papavasiliou, F. Nina
Abstract	Activation-induced cytidine deaminase (AID) is expressed in germinal centers of lymphoid organs during immunoglobulin diversification, in bone marrow B cells after infection with Abelson murine leukemia retrovirus (Ab-MLV), and in human B cells after infection by hepatitis C virus. To understand how viruses signal AID induction in the host we asked whether the AID response was abrogated in cells deficient in the interferon pathway or in signaling via the Toll-like receptors. Here we show that AID is not an interferon responsive gene and abrogation of Toll-like receptor signaling does not diminish the AID response. However, we found that NF-κB was required for expression of virally induced AID. Since NF-κB binds and activates the AID promoter, these results mechanistically link viral infection with AID transcription. Thus, induction of AID by viruses could be the result of several signaling pathways that culminate in NF-κB activation, underscoring the versatility of this host defense program.
Related Links	http://dx.doi.org/10.1084/jem.20061801
Starting Page	259
File Format	PDF
ISSN	15409538
e-ISSN	15409538
Journal	The Journal of Experimental Medicine
Issue Number	2
Volume Number	204
Language	English
Publisher	The Rockefeller University Press
Publisher Date	2007-02-19
Access Restriction	Open
Rights Holder	The Rockefeller University Press
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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