AKTivation of PI3K/AKT/mTOR signaling pathway by KSHV

被引：102

作者：

Bhatt, Aadra P. ^{[1
,2
]}

Damania, Blossom ^{[1
,2
]}

机构：

[1] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA

[2] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA

来源：

FRONTIERS IN IMMUNOLOGY | 2013年 / 3卷

关键词：

Akt; KSHV; mTOR; PI3K; B cells; SARCOMA-ASSOCIATED-HERPESVIRUS; PROTEIN-COUPLED-RECEPTOR; PRIMARY EFFUSION LYMPHOMA; NF-KAPPA-B; MULTICENTRIC CASTLEMANS-DISEASE; PRIMARY ENDOTHELIAL-CELLS; FOCAL ADHESION KINASE; RIBOSOMAL S6 KINASE; KAPOSIS-SARCOMA; NUCLEAR ANTIGEN;

D O I：

10.3389/fimmu.2012.00401

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

As an obligate intracellular parasite, Kaposi sarcoma-associated herpesvirus (KSHV) relies on the host cell machinery to meet its needs for survival, viral replication, production, and dissemination of progeny virions. KSHV is a gammaherpesvirus that is associated with three different malignancies: Kaposi sarcoma (KS), and two B cell lymphoproliferative disorders, primary effusion lymphoma (PEL) and multicentric Castleman's disease. KSHV viral proteins modulate the cellular phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway, which is a ubiquitous pathway that also controls B lymphocyte proliferation and development. We review the mechanisms by which KSHV manipulates the PI3K/AKT/mTOR pathway, with a specific focus on B cells.

引用

页数：16

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