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Preparation of transgenic Iranian lizard Leishmania coding HIL-12.

Leishmania are intracellular flagellate protozoan parasites cause a wide spectrum of clinical manifestations in human. The immunological basis for resistance against leishmaniasis depends on Thl responses in the course of performance of cytokines like IL-12. In this study, a transgenic Leishmania coding human IL-12 was produced that can be used in Leishmanization.

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Regnase-1 and Roquin Nonredundantly Regulate Th1 Differentiation Causing Cardiac Inflammation and Fibrosis.

Regnase-1 and Roquin are RNA binding proteins that are essential for degradation of inflammatory mRNAs and maintenance of immune homeostasis. Although deficiency of either of the proteins leads to enhanced T cell activation, their functional relationship in T cells has yet to be clarified because of lethality upon mutation of both Regnase-1 and Roquin. By using a Regnase-1 conditional allele, we show that mutations of both Regnase-1 and Roquin in T cells leads to massive lymphocyte activation. In contrast, mutation of either Regnase-1 or Roquin affected T cell activation to a lesser extent than the double mutation, indicating that Regnase-1 and Roquin function nonredundantly in T cells. Interestingly, Regnase-1 and Roquin double-mutant mice suffered from severe inflammation and early formation of fibrosis, especially in the heart, along with the increased expression of Ifng, but not Il4 or Il17a Consistently, mutation of both Regnase-1 and Roquin leads to a huge increase in the Th1, but not the Th2 or Th17, population in spleens compared with T cells with a single Regnase-1 or Roquin deficiency. Regnase-1 and Roquin are capable of repressing the expression of a group of mRNAs encoding factors involved in Th1 differentiation, such as Furin and Il12rb1, via their 3' untranslated regions. Moreover, Regnase-1 is capable of repressing Roquin mRNA. This cross-regulation may contribute to the synergistic control of T cell activation/polarization. Collectively, our results demonstrate that Regnase-1 and Roquin maintain T cell immune homeostasis and regulate Th1 polarization synergistically.

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Moxifloxacin Modulated TGF-β1-Related Interleukin-12 Secretion in Corneal Fibroblasts.

To explore the variability in interleukin-12 (IL-12) secretion in human corneal fibroblasts (HCFs), the effects of IL-12 on HCF viability and migration, and the effects of recombinant human transforming growth factor-β1 (rhTGF-β1) and moxifloxacin (MOX) on IL-12 expression.

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Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Recombinant Rat Interleuk Recombinant Rat Interleuk Recombinant Rat Interleuk Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle Rat monoclonal anti mouse

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Paracoccidioidomycosis Associated With a Heterozygous STAT4 Mutation and Impaired IFN-γ Immunity.

Mutations in genes affecting interferon-γ (IFN-γ) immunity have contributed to understand the role of IFN-γ in protection against intracellular pathogens. However, inborn errors in STAT4, which controls interleukin-12 (IL-12) responses, have not yet been reported. Our objective was to determine the genetic defect in a family with a history of paracoccidioidomycosis.

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STAT4 (Phospho Tyr693) An Androgen Receptor (Phosph Androgen Receptor (Phosph Mouse Anti-Human IFN-alph Mouse Anti-Human IFN-alph Mouse Anti-Human IFN-alph Mouse Anti-Human IFN-alph Mouse Anti-Human IFN-beta Mouse Anti-Human IFN-beta Rat Anti-Mouse IFN-gamma Rat Anti-Mouse IFN-gamma Mouse Anti-Human IFN-gamm

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IL-12 induces autophagy in human breast cancer cells through AMPK and the PI3K/Akt pathway.

Interleukin-12 (IL-12) serves an important role in immune responses and antitumor activity. The study of the association between autophagy and cancer cells remains controversial. The present study aimed to investigate the effect of IL‑12 on autophagy in the human breast cancer cell lines MDA‑MB‑231 and MCF‑7, and the possible molecular mechanism. Breast cancer cells were treated with different concentrations of recombinant IL‑12. The expression of the autophagy-associated protein microtubule‑associated protein light chain 3 (LC3) was determined using western blot analysis, fluorescein isothiocyanate‑labeled LC3 was detected using fluorescence microscopy and autophagosomes were examined using transmission electron microscopy. Alterations in the phosphatidylinositol 3‑kinase/Rac‑α serine/threonine protein kinase (PI3K/Akt) and 5'‑AMP‑activated protein kinase subunit β‑1 (AMPK) pathways, in addition to pathway‑associated proteins, were detected using western blotting, following treatment with IL‑12 and pretreatment with the PI3K/Akt activator insulin‑like growth factor or the AMPK inhibitor compound C. It was observed that IL‑12 was able to upregulate the expression of the autophagy‑associated protein LC3 in a concentration‑ and time‑dependent manner, and induce the formation of autophagosomes in the two cell lines, and that the above effects involved the inhibition of the PI3K/Akt signaling pathway and the activation of the AMPK signaling pathway.

2892 related Products with: IL-12 induces autophagy in human breast cancer cells through AMPK and the PI3K/Akt pathway.

Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle Breast cancer tissue arra Breast cancer tissue arra Human breast invasive duc Breast cancer test tissue Breast cancer test tissue Breast cancer test tissue Top 4 types of cancer (co CELLKINES Natural Human I

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[Oncolytic property of HSV-1 recombinant viruses carrying the human IL-12].

Objective: Constructed the recombinant HSV-1 deleted ICP47 and inserted human IL-12, and investigate the virus' replication ability and oncolytic property in vitro and vivo. Methods: The recombinant HSV-1 deleting ICP47 (MH1005) and then inserting human IL-12 (MH1006) were obtained with bacterial artificial chromosome technology.The replication ability and the efficiency of inhibiting tumor were detected in several nerve tumor cell lines infected with HSV-wt, MH1005 and MH1006 respectively.The murine tumor model was established by subcutaneous inoculation Neuro-2a cells on both sides of mice back respectively.A dosage of 2×10(6) PFU of HSV-wt, MH1001(recombinant HSV-1 deleted IR), MH1005, MH1006 and Mock were injected 3 times intratumorally on one side of mice back in every 3 days, the tumor volume and survival rate of the mice were measured. Results: The replication abilities of MH1005, MH1006 and HSV-wt in 293FT cells were insignificant (P>0.05); the replication abilities of recombinant HSV-1 in G422 and Neuro-2a were higher than that in SK-N-SH; and the nerve tumor cells could be inhibited significantly by recombinant HSV-1.After 15 days of treatment, on the mouse backside with injection treatment, the tumor volumes of group HSV-wt (6 267±484), MH1001 (5 730±1 071), MH1005 (4 537±538)and MH1006 (4 150±476)mm(3) were smaller than that of group Mock (6 957±722) mm(3) significantly (all P<0.01); on the mouse backside without injection treatment, the tumor volumes of group MH1005 (5 952±607) and MH1006 (5 473±661) mm(3) were smaller than those of HSV-wt (6 785±1 063), MH1001 (6 774±808) and Mock (6 957±190) mm(3) significantly (all P<0.05); after 35 days of treatment, the mice survival rates of group MH1005 (100%) and MH1006 (100%) were higher than those of MH1001 (67%), HSV-wt (50%) and Mock (33%) significantly (all P<0.05). Conclusion: MH1005 and MH1006 can infect nerve tumor cells and replicate at high level, the viruses not only kill tumor cells directly but also induce immunological rejection to tumor, and prolong the survival of mice bearing tumor.

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Recombinant Human Interle Recombinant Human Interle Recombinant Human IL-12 p Recombinant Human Interle Recombinant Human Interle Recombinant Human IL-12 p IL 12, human recombinant IL-12, human recombinant IL-12 Receptor beta2 anti Recombinant Human IL-1 al Recombinant Human IL-1 al Recombinant Human IL-1 al

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Suppression of IL-12p70 formation by IL-2 or following macrophage depletion causes T-cell autoreactivity leading to CNS demyelination in HSV-1-infected mice.

We have established two mouse models of central nervous system (CNS) demyelination that differ from most other available models of multiple sclerosis (MS) in that they represent a mixture of viral and immune triggers. In the first model, ocular infection of different strains of mice with a recombinant HSV-1 that expresses murine IL-2 constitutively (HSV-IL-2) causes CNS demyelination. In the second model, depletion of macrophages causes CNS demyelination in mice that are ocularly infected with wild-type (WT) HSV-1. In the present study, we found that the demyelination in macrophage-intact mice infected with HSV-IL-2 was blocked by depletion of FoxP3-expressing cells, while concurrent depletion of macrophages restored demyelination. In contrast, demyelination was blocked in the macrophage-depleted mice infected with wild-type HSV-1 following depletion of FoxP3-expressing cells. In macrophage-depleted HSV-IL-2-infected mice, demyelination was associated with the activity of both CD4+ and CD8+ T cells, whereas in macrophage-depleted mice infected with WT HSV-1, demyelination was associated with CD4+ T cells. Macrophage depletion or infection with HSV-IL-2 caused an imbalance of T cells and TH1 responses as well as alterations in IL-12p35 and IL-12p40 but not other members of the IL-12 family or their receptors. Demyelination was blocked by adoptive transfer of macrophages that were infected with HSV-IL-12p70 or HSV-IL-12p40 but not by HSV-IL-12p35. These results indicate that suppression of IL-12p70 formation by IL-2 or following macrophage depletion causes T-cell autoreactivity leading to CNS demyelination in HSV-1-infected mice.

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anti HSV (II) gB IgG1 (mo CELLKINES Natural Human I Human Interleukin-7 IL-7 Human Interleukin-16 IL-1 Human Interleukin-33 IL-3 Human Interleukin-17E (IL Human Interleukin-32 alph Human Epstein-Barr Virus Human Interleukin-1-beta Human Interleukin-29 IL-2 Human Interleukin-1-alpha Human Interleukin-3 IL-3

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Altered Natural Killer Cell Function in HIV-Exposed Uninfected Infants.

HIV-exposed uninfected (HEU) infants have higher rates of severe and fatal infections compared with HIV-unexposed (HUU) infants, likely due to immune perturbations. We hypothesized that alterations in natural killer (NK) cell activity might occur in HEU infants and predispose them to severe infections.

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Study of recombinant human interleukin-12 for treatment of complications after radiotherapy for tumor patients.

To evaluate the treatment effects of recombinant human interleukin-12 (rhIL-12) on radiotherapy complications, such as severe myelosuppression or pancytopenia, the decline or imbalance of immune function, etc.

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Hepatitis C virus impairs natural killer cell activity via viral serine protease NS3.

Hepatitis C virus (HCV) infection is characterized by a high frequency of chronic cases owing to the impairment of innate and adaptive immune responses. The modulation of natural killer (NK) cell functions by HCV leads to an impaired innate immune response. However, the underling mechanisms and roles of HCV proteins in this immune evasion are controversial, especially in the early phase of HCV infection. To investigate the role of HCV nonstructural proteins especially NS3 in the impairment of NK functions, NK cells were isolated from the PBMCs by negative selection. To assess the direct cytotoxicity and IFN-γ production capability of NK cells, co-cultured with uninfected, HCV-infected, HCV-NS3 DNA-transfected Huh-7.5, or HCV-NS replicon cells. To determine the effect of an NS3 serine protease inhibitor, HCV-infected Huh-7.5 cells were treated with BILN-2061. Then, NK cells were harvested and further co-cultured with K-562 target cells. NK cell functions were analyzed by flow cytometry and enzyme-linked immunosorbent assay. When co-cultured with HCV-infected Huh-7.5 cells, the natural cytotoxicity and IFN-γ production capability of NK cells were significantly reduced. NK cell functions were inhibited to similar levels upon co-culture with HCV-NS replicon cells, NS3-transfected cells, and HCV-infected Huh-7.5 cells. These reductions were restored by BILN-2061-treatment. Furthermore, BILN-2061-treatment significantly increased degranulation against K-562 target cells and IFN-γ productivity in NK cells. Consistent with these findings, the expression levels of activating NK cell receptors, such as NKp46 and NKp30, were also increased. In HCV-infected cells, the serine protease NS3 may play a role in the abrogation of NK cell functions in the early phase of infection through downregulation of NKp46 and NKp30 receptors on NK cells. Together, these results suggest that NS3 represents a novel drug target for the treatment of HCV infections.

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