TUMOR NECROSIS FACTOR-α DRIVES HIV-1 REPLICATION IN U937 CELL CLONES AND UPREGULATES CXCR4

Biswas, Priscilla; Mantelli, Barbara; Delfanti, Fanny; Cota, Manuela; Vallanti, Giuliana; Filippi, Camilla De; Mengozzi, Manuela; Vicenzi, Elisa; Lazzarin, Adriano; Poli, Guido

doi:10.1006/cyto.2000.0798

Cited by 24 publications

(16 citation statements)

References 13 publications

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“…IL-6 induces monocyte chemotactic protein-1 (MCP-1) from monocytes and the IL-6/IL-6R complex induces MCP-1 and adhesion molecules, ICAM-1 in endothelial cells. 12,13) These lines of evidence support the idea that the IL-6 system plays a positive role in the local inflammatory reaction by amplifying inflammatory cell infiltration. Furthermore, angiogenesis is a characteristic feature of RA synovium.…”

Section: Discussionsupporting

confidence: 56%

Tocilizumab, a Humanized Anti-interleukin-6 Receptor Antibody, Ameliorates Joint Swelling in Established Monkey Collagen-Induced Arthritis

Uchiyama

Yorozu

Hashizume

et al. 2008

Biological & Pharmaceutical Bulletin

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Section: Discussionsupporting

confidence: 56%

Tocilizumab, a Humanized Anti-interleukin-6 Receptor Antibody, Ameliorates Joint Swelling in Established Monkey Collagen-Induced Arthritis

Uchiyama

Yorozu

Hashizume

et al. 2008

Biological & Pharmaceutical Bulletin

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“…7). Of note, U937 Plus cells display constitutive mRNA for TNF- § (but not for IL-1 g nor IL-6), which is also spontaneously secreted [31]. However, its concentration in this SN was not sufficient to induce HIV expression, whereas secreted sTNFR1 may be related to the partial inhibition of TNF- § -induced RT activity (Fig.…”

Section: Scd30-containing Supernatant Specifically Inhibits the Up-rementioning

confidence: 91%

CD30 ligation differentially affects CXCR4‐dependent HIV‐1 replication and soluble CD30 secretion in non‐Hodgkin cell lines and in γ δ T lymphocytes

et al. 2003

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We studied whether signaling through CD30, a member of the TNF receptor family, affected acute infection with HIV-1, encompassing its entire replicative cycle. Several non-Hodgkin cell lines, targets of CXCR4-dependent (X4) HIV-1 infection, were positive for CD30 expression. CD30 ligation induced up-regulation of viral replication only in certain CD30 + cell lines. Enhancement of X4 virus replication by CD30 engagement inversely correlated with both CD30 surface density and constitutive NF-‹ B activation. Conversely, expression of CD30, but not of other members of the TNF receptor family, was proportional to constitutive NF-‹ B binding. Concomitantly, secretion of soluble (s) CD30 increased in all cell lines by CD30 ligation. sCD30 release was enhanced by engagement of CD30 alone and, to a greater extent, by co-engagement of CD3 also in primary +ˇT lymphocytes, along with complementary modulations of their surface CD30 expression. sCD30-containing supernatant specifically inhibited HIV-1 expression induced by CD30 engagement in chronically infected ACH-2 T cells; thus sCD30 may act as a negative feed-back molecule. In conclusion, we have delineated novel features of CD30 biology and underline the peculiar link of CD30 expression to constitutive NF-‹ B activation which is pivotal to both HIV replication and cell survival.

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“…Promonocytic U937 cell clones were previously defined as ''plus'' or ''minus'' in relationship to their efficient or inefficient capacity to sustain CXCR4-dependent (X4) HIV-1 LAI/IIIB replication (16)(17)(18). The U1 cell line was originally obtained from a population of U937 cells surviving the cytopathic effect of acute HIV-1 LAI/IIIB infection and contains two copies of integrated provirus (19).…”

Section: Methodsmentioning

confidence: 99%

“…To investigate whether uPAuPAR interaction could interfere with acutely infected cells, we first determined their levels of expression in promonocytic cell clones of the U937 cell line (parental to U1 cells), previously characterized in terms of their efficient (plus clones) or poor (minus clones) capacity to sustain X4 HIV-1 replication (16,18). Plus cells (U937-SB and clone 10) expressed lower levels of both uPAR and CD11b͞CD18 than minus cells (clone 12 and 34) at the cell surface (Fig.…”

Section: Inhibitory Effects Of Pro-upa On Acute Hiv-1 Replication In mentioning

confidence: 99%

Urokinase–urokinase receptor interaction mediates an inhibitory signal for HIV-1 replication

Alfano

Sidénius

Panzeri

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Elevated levels of soluble urokinase-type plasminogen activator (uPA) receptor, CD87͞u-PAR, predict survival in individuals infected with HIV-1. Here, we report that pro-uPA (or uPA) inhibits HIV-1 expression in U937-derived chronically infected promonocytic U1 cells stimulated with phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-␣ (TNF-␣). However, pro-uPA did not inhibit PMA or TNF-␣-dependent activation of nuclear factor-kB or activation protein-1 in U1 cells. Cell-associated HIV protein synthesis also was not decreased by pro-uPA, although the release of virion-associated reverse transcriptase activity was substantially inhibited, suggesting a functional analogy between pro-uPA and the antiviral effects of IFNs. Indeed, cell disruption reversed the inhibitory effect of pro-uPA on activated U1 cells, and ultrastructural analysis confirmed that virions were preferentially retained within cell vacuoles in pro-uPA treated cells. Neither expression of endogenous IFNs nor activation of the IFN-inducible Janus kinase͞ signal transducer and activator of transcription pathway were induced by pro-uPA. Pro-uPA also inhibited acute HIV replication in monocyte-derived macrophages and activated peripheral blood mononuclear cells, although with great inter-donor variability. However, pro-uPA inhibited HIV replication in acutely infected promonocytic U937 cells and in ex vivo cultures of lymphoid tissue infected in vitro. Because these effects occurred at concentrations substantially lower than those affecting thrombolysis, pro-uPA may represent a previously uncharacterized class of antiviral agents mimicking IFNs in their inhibitory effects on HIV expression and replication.

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TUMOR NECROSIS FACTOR-α DRIVES HIV-1 REPLICATION IN U937 CELL CLONES AND UPREGULATES CXCR4

Cited by 24 publications

References 13 publications

Tocilizumab, a Humanized Anti-interleukin-6 Receptor Antibody, Ameliorates Joint Swelling in Established Monkey Collagen-Induced Arthritis

Tocilizumab, a Humanized Anti-interleukin-6 Receptor Antibody, Ameliorates Joint Swelling in Established Monkey Collagen-Induced Arthritis

CD30 ligation differentially affects CXCR4‐dependent HIV‐1 replication and soluble CD30 secretion in non‐Hodgkin cell lines and in γ δ T lymphocytes

Urokinase–urokinase receptor interaction mediates an inhibitory signal for HIV-1 replication

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