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Inflammatory Cytokines and HIV-1-Associated Neurodegeneration . . . The results indicated that inflammatory cytokines such as TNF-α, TNF-β, IL-6, IL-1α, IL-1β, IFN-γ, or TGF-β1 did not alter cell viability and morphology, although they variably stimulated neuronal cell proliferation (Fig 2A)
Insights into the HIV Latency and the Role of Cytokines - MDPI TGF-β regulates HIV replication directly by acting on infected cells; however, TGF-β can either stimulate or inhibit HIV replication, unlike monophasic stimulation of HIV replication by cytokines (i e , IL-1, TNF-α, GM-CSF, LIF) or monophasic inhibition in response to interferons
Advanced in immunological monitoring of HIV infection: profile of . . . As the ratio of CD4 CD8 T cells has always been so far, the present study shows that NK and NKT cells as well as IL-6, TNF-α, IL-5 and IL-7 cytokines could be valuable additional immunological biomarkers in the therapeutic monitoring of PLHIV-1
Cytokines and HIV-1: Interactions and Clinical Implications Increased production of proinflammatory cytokines (IL-1, IL-6, IL-8 and TNF-α) are also thought to activate HIV-1 replication and maintain active HIV-1 expression via binding of NF-κB to LTR
Profiling HIV1-host protein–protein interaction networks in patient . . . Notably, the Nef protein aids in evading the innate immune response through (i) upregulating proinflammatory cytokines expression, such as IL-1β, IL-12, IL-15, and TNF-α, as well as chemokines like macrophage inflammatory protein (MIP)-1α, -1β, and IL-8 [24, 25] (ii) precisely, HIV-1 Nef act as a tetherin antagonist and reduces NK cell
HIV Antigens Can Induce TGF-β 1 -Producing Immunoregulatory CD8 + T Cells 1 HIV-infected individuals may progressively lose both HIV-specific and unrelated CTL responses despite the high number of circulating CD8 + T cells In this study, we report that ∼25% of HIV + donors produced TGF-β 1 in response to stimulation with HIV proteins or peptides