155971-7124

pubmed-article:10964543, pubmed-article:11602715, pubmed-article:12089333, pubmed-article:12372982, pubmed-article:1380260, pubmed-article:15288392, pubmed-article:15307952, pubmed-article:15481145, pubmed-article:1548758, pubmed-article:16160188, pubmed-article:16313253, pubmed-article:16621960, pubmed-article:16846840, pubmed-article:17030448, pubmed-article:17360657, pubmed-article:18649336, pubmed-article:18670216, pubmed-article:18826950, pubmed-article:1905933, pubmed-article:1918997, pubmed-article:1918999, pubmed-article:1993354, pubmed-article:20083573, pubmed-article:20121167, pubmed-article:20380698, pubmed-article:20817073, pubmed-article:21948112, pubmed-article:22340390, pubmed-article:22463742, pubmed-article:22496218, pubmed-article:22528837, pubmed-article:22591361, pubmed-article:22814248, pubmed-article:7511078, pubmed-article:7536422, pubmed-article:7561697, pubmed-article:7704970, pubmed-article:7706435, pubmed-article:7815507, pubmed-article:8267288, pubmed-article:8336118, pubmed-article:8381971, pubmed-article:8482849, pubmed-article:8707350, pubmed-article:8764000, pubmed-article:8806809, pubmed-article:8870842, pubmed-article:9108403, pubmed-article:9223523, pubmed-article:9225992, pubmed-article:9226228, pubmed-article:9269777, pubmed-article:9344703, pubmed-article:9658081, pubmed-article:9744279

Apoptosis of CD8+ cells is mediated by the interaction between TNF-alpha bound to the membrane of macrophages (mbTNF) and a receptor on CD8+ T cells (TNF-receptor II, or TNFRII), which is upregulated by treatment with recombinant HIV-1 gp120 or SDF-1, B cells from peripheral blood and lymph nodes of HIV-infected individuals secrete significant levels of TNF-alpha in the presence of HIV-1 gp120, CD4 downregulation by the treatment of macrophages with HIV-1 gp120 is mediated through the induction of endogenous TNF-alpha, Cytokines induced in vitro by HIV-1 gp120 in normal peripheral blood mononuclear cells (PBMC) include interferon-alpha (IFN-alpha) and IFN-gamma, tumor necrosis factor-alpha (TNF-alpha), IL-6, IL-10, IL-1 alpha and IL1 beta, Enhanced TNF-alpha responses are observed when peripheral blood mononuclear cells (PBMCs) are costimulated with HIV-1 gp120 and mannose-binding lectin (MBL), Exposure of macrophages to purified CCR5- or CXCR4-tropic HIV-1 envelope glycoprotein gp120 induces secretion of high levels of macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, RANTES, and tumor necrosis factor alpha, Frequent IFN-gamma and TNF-alpha NK cell responses to HIV-1 gp120 are dominant during chronic HIV-1 infection, Genistein, tyrosine kinase inhibitor, suppresses HIV-1 gp120-induced TNF-alpha secretion by primary macrophage, HIV gp120 and TNF-alpha synergistically reduce endothelial nitric oxide synthase (eNOS) expression and cause endothelial dysfunction via ICAM-1, HIV-1 gp120 enhances TNF-a-induced VCAM-1 gene expression in coronary macrovascular endothelial cells, HIV-1 gp120 induces human glial cells to release more TNF-alpha and IL-1beta than untreated cells, HIV-1 gp120 inhibits CpG-A-induced secretion of TNF-a, IL-6, and IP-10 proteins in plasmacytoid dendritic cells and PBMCs, HIV-1 gp120 inhibits TLR9-mediated upregulation of CD83 and the secretion of inflammatory cytokines TNF-alpha and IL-6, and chemokine IP10 in plasmacytoid dendritic cells (pDC), HIV-1 gp120 partially inhibits the negative beta-adrenergic modulation of lipopolysaccharide-induced production of tumor necrosis factor alpha in microglial cells, HIV-1 gp120 stimulates human cells to release TNF-alpha, IL-1 beta, IL-6, and granulocyte-macrophage-CSF, and this effect can be blocked with soluble CD4, HIV-1 gp120 stimulates the release of TNF-alpha from TPA-differentiated HL-60 cells; treatment with TNF-alpha neutralizing antibody and anti-TNF-alpha receptor type II (TNFR-II) antibody, inhibits gp120-induced upregulation of mu opioid receptor, HIV-1 gp120 triggers apoptosis in primary osteoblasts and osteoblast-derived cell lines (HOBIT) through TNFalpha activation, HIV-1 gp160-induced apoptosis is affected in part by the release of TNF-alpha and is associated with attenuated Bcl-2 mRNA expression, HIV-1 gp41 or gp120 synthetic peptides induce the production of interleukin (IL)-1 and tumor necrosis factor (TNF); in contrast, gp41 or gp120 synthetic peptides are able to depress the production of interferon (IFN)-alpha, IFN-gamma, and IL-2, HIV-1 gp41 stimulates microglial cell production of cytokines (TNF-alpha, IL-1beta, and IL-6) and chemokines (RANTES and MIP-1alpha), In CD4-positive Jurkat cells, HIV-1 gp120 enhances TNF-induced NF-kappa B activation, Inhibition of NRF2 by siRNA results in increased NOX2, NFkappaB (p65/p50), TNF-alpha, and MMP-9 proteins in astrocytes exposed to HIV-1 gp120, NK cells that respond with IFN-gamma and TNF-alpha cytokine production to HIV-1 gp120 peptides have reduced CD16 and NKp46 expression and have increased levels of CD57, Pretreatment of CD4+ T cells with HIV-1 gp160 results in marked inhibition of TNF-alpha secretion, Pretreatment of HIV-1 infected cells with TNF alpha augments syncytia formation mediated by the interaction of HIV-1 gp120 with cell surface CD4 molecules, Pretreatment of cells with HIV-1 gp160 results in marked inhibition of tyrosine phosphorylation of p59(fyn), PLC-gamma1, ras activation, and TNF-alpha secretion in anti-CD3 mAb activated CD4+ T cells, Stimulation of human monocyte-derived macrophages with HIV-1 gp120 results in the CCR5-mediated activation of Lyn and the concomitant Lyn-dependent activation of the mitogen-activated protein (MAP) kinase ERK-1/2, which leads to production of TNF-alpha, Treatment of HIV-1-infected monocytes with TNF-alpha increases the sensitivity of the interaction of the HIV-1 antigen gp120 with cytotoxic sera from HIV-1 infected individuals