Programmed death-1 receptor negatively regulates LPS-mediated IL-12 production and differentiation of murine macrophage RAW264.7 cells

Cho, Hae-Yun; Choi, Eun Seo; Lee, Soo-Woon; Jung, Keunok; Seo, Su‐Kil; Choi, Il‐Whan; Park, Sae-Gwang; Choi, Inhak; Lee, Soo-Woong

doi:10.1016/j.imlet.2009.08.011

Cited by 46 publications

(57 citation statements)

References 32 publications

(40 reference statements)

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“…Recently, it was demonstrated that, in addition to T and B lymphocytes, PD-1 can be induced on murine macrophages or DCs by bacterial infection or TLR engagement, and SOCS-1 negatively regulates IL-12 production in a murine model (23)(24)(25)(26). We previously showed that HCV core protein regulates T and B lymphocyte activation and M/M F IL-12 production through interaction with a complement receptor (gC1qR) (27)(28)(29)(30)(31)(32)(33).…”

Section: Discussionmentioning

confidence: 99%

“…For example, PD-1 was found to be upregulated on exhausted CD4 + and CD8 + T cells during chronic HCV infection (21,22). PD-1 and SOCS-1 were also shown to regulate murine monocyte IL-10/IL-12 production against bacterial infection (23)(24)(25)(26). Similarly, we demonstrated that HCV core protein, by interaction with a complement receptor (gC1qR), can differentially regulate T and B lymphocyte functions through modulating PD-1/SOCS-1 signaling (27)(28)(29)(30)(31)(32).…”

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confidence: 99%

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Cross-Talk between Programmed Death-1 and Suppressor of Cytokine Signaling-1 in Inhibition of IL-12 Production by Monocytes/Macrophages in Hepatitis C Virus Infection

Zhang

Cheng

et al. 2011

The Journal of Immunology

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Hepatitis C virus (HCV) dysregulates innate immune responses and induces persistent viral infection. We previously demonstrated that HCV core protein impairs IL-12 expression by monocytes/macrophages (M/MΦs) through interaction with a complement receptor gC1qR. Because HCV core-mediated lymphocyte dysregulation occurs through the negative immunomodulators programmed death-1 (PD-1) and suppressor of cytokine signaling-1 (SOCS-1), the aim of this study was to examine their role in HCV core-mediated IL-12 suppression in M/MΦs. We analyzed TLR-stimulated, primary CD14+ M/MΦs from chronically HCV-infected and healthy subjects or the THP-1 cell line for PD-1, SOCS-1, and IL-12 expression following HCV core treatment. M/MΦs from HCV-infected subjects at baseline exhibited comparatively increased PD-1 expression that significantly correlated with the degree of IL-12 inhibition. M/MΦs isolated from healthy and HCV-infected individuals and treated with HCV core protein displayed increased PD-1 and SOCS-1 expression and decreased IL-12 expression, an effect that was also observed in cells treated with gC1qR’s ligand, C1q. Blocking gC1qR rescued HCV core-induced PD-1 upregulation and IL-12 suppression, whereas blocking PD-1 signaling enhanced IL-12 production and decreased the expression of SOCS-1 induced by HCV core. Conversely, silencing SOCS-1 expression using small interfering RNAs increased IL-12 expression and inhibited PD-1 upregulation. PD-1 and SOCS-1 were found to associate by coimmunoprecipitation studies, and blocking PD-1 or silencing SOCS-1 in M/MΦ led to activation of STAT-1 during TLR-stimulated IL-12 production. These data suggested that HCV core/gC1qR engagement on M/MΦs triggers the expression of PD-1 and SOCS-1, which can associate to deliver negative signaling to TLR-mediated pathways controlling expression of IL-12, a key cytokine linking innate and adaptive immunity.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Cross-Talk between Programmed Death-1 and Suppressor of Cytokine Signaling-1 in Inhibition of IL-12 Production by Monocytes/Macrophages in Hepatitis C Virus Infection

Zhang

Cheng

et al. 2011

The Journal of Immunology

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“…It is also known that IFX treatment robustly downregulates the relative expression of the IL-6 and CCL1 genes in Staphylococcus aureus-derived peptidoglycan stimulated primary human dendritic cells [41]. The interesting, opposing effects of both IFX and IgG on PDCD1 expression of PMA-and LPS-stimulated cells should be further investigated, as this receptor seems to play an important role in the polarization of macrophages [42] and immune suppression.…”

Section: Discussionmentioning

confidence: 99%

Reverse Signaling Contributes to Control of Chronic Inflammation by Anti-TNF Therapeutics

et al. 2015

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Anti-tumor necrosis factor (TNF) monoclonal antibodies and TNF receptor ectodomain fusion protein are in clinical use to neutralize circulating TNF and ameliorate symptoms of many autoimmune diseases and pathological conditions with chronic inflammation. In this paper we present data to prove that reverse signaling, elicited by agonist molecules interacting with the membrane-bound TNF of myeloid cells, significantly contributes to the therapeutic effect of these anti-TNF medicines. Interaction of agonist monoclonals with cell surface TNF significantly attenuates the expression of pro-inflammatory cytokines and induces changes in the production of extracellular and intracellular signaling molecules. This phenomenon is not dependent on the Fc portion of antibodies as Fab constructs are as efficient as full antibody molecules.

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“…Cell lines (RAW264.7, Mouse D3 and F9 ES, EMT6) were cultured according to previously described protocols (Brandt 2010;Cho et al 2009;Estes et al 1997;Thompson & Gudas 2002). Cells were cultured at 37…”

Section: Cell Culturementioning

confidence: 99%

Expression patterns of Nlrp9a, Nlrp9b and Nlrp9c during mouse development

et al. 2013

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Abstract:The Nlrp gene family contains 20 members in the mouse. Recent studies have demonstrated that these genes play key roles in reproduction. In this study, we investigated the expression patterns of Nlrp9a, Nlrp9b and Nlrp9c in the mouse. In 2-week-old mouse tissues, Nlrp9a, Nlrp9b and Nlrp9c were all strikingly expressed in the ovary, while the transcripts of Nlrp9b and Nlrp9c were also detected in other tissues. The transcripts of Nlrp9a, Nlrp9b and Nlrp9c were restricted to the oocytes and declined with oocyte aging within the ovary. Furthermore, Nlrp9a, Nlrp9b and Nlrp9c transcripts presented evidence for the exclusive maternal origin, which were presented in oocytes and zygotes, immediately downregulated and not detected after the 2-cell stage during preimplantation development. In addition, Nlrp9a and Nlrp9c transcripts were not detected in other cells except for oocytes. Nevertheless, Nlrp9b expression was detected in oocytes, as well as in D3 ES and F9 ES. These results indicate that Nlrp9a, Nlrp9b and Nlrp9c display specific or preferential oocyte expression patterns and may play critical role in oogenesis and/or preimplantation embryo development in the mouse.

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Programmed death-1 receptor negatively regulates LPS-mediated IL-12 production and differentiation of murine macrophage RAW264.7 cells

Cited by 46 publications

References 32 publications

Cross-Talk between Programmed Death-1 and Suppressor of Cytokine Signaling-1 in Inhibition of IL-12 Production by Monocytes/Macrophages in Hepatitis C Virus Infection

Cross-Talk between Programmed Death-1 and Suppressor of Cytokine Signaling-1 in Inhibition of IL-12 Production by Monocytes/Macrophages in Hepatitis C Virus Infection

Reverse Signaling Contributes to Control of Chronic Inflammation by Anti-TNF Therapeutics

Expression patterns of Nlrp9a, Nlrp9b and Nlrp9c during mouse development

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