Open AccessCasp8p41 expression in primary T cells induces a proinflammatory response
Author(s) -
Julie Taylor,
Nathan W. Cummins,
Gary D. Bren,
Stacey A. Rizza,
Christopher P. Kolbert,
Marshall D. Behrens,
Keith L. Knutson,
Jane Kahl,
Yan W. Asmann,
Andrew D. Badley
Publication year - 2010
Publication title -
aids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.195
H-Index - 216
eISSN - 1473-5571
pISSN - 0269-9370
DOI - 10.1097/qad.0b013e3283389e90
Subject(s) - proinflammatory cytokine , biology , cytokine , flow cytometry , tumor necrosis factor alpha , microbiology and biotechnology , apoptosis , immunology , inflammation , biochemistry
HIV infection of CD4 T cells can lead to HIV protease-mediated cleavage of procaspase 8 generating a novel, HIV-specific peptide called Casp8p41. Casp8p41 has at least two biologic functions: induction of cell death via mitochondrial depolarization and release of cytochrome C, as well as activation of nuclear factor kappa B (NFkappaB). We have previously shown that Casp8p41-induced NFkappaB activation enhances HIV LTR transcription and consequently increases HIV replication. Herein, we questioned whether Casp8p41-induced NFkappaB activation impacts the cytokine profile of cells expressing Casp8p41.