Impaired interferon-α expression in plasmacytoid dendritic cells in asthma

Impaired interferon-α expression in plasmacytoid dendritic cells in asthma

Background: Activation of the receiver receiver (RV) is involved in the pathogenesis of asthma. The dendritic cells of plasmacytoids (PDCs) are the main interferon-α cells against viruses.

OBJECTIVE: To determine whether asthmatic patients and control topics differ in terms of interferon-α expression in PDCs under TLR-7 or RV stimulation.

Methods: PDCs have been identified in mononuclear cells of BDCA-2 + and HLA-DR + peripheral blood. The interferon-α expression of the PDC was analyzed after the TLR-7 stimulation with or without interleukin (IL-4) / pretreatment IL-13. Interferon-α expression was also analyzed after RV stimulation over periods of 24, 48 or 96 hours with or without pretreatment IL-4. RV detection and molecular typing have been analyzed from throat swabs.

Results: Following the TLR-7 stimulation, the expression of intracellular-α interferon was higher in the PDCs of normal subjects than those of asthmatic patients; However, pretreatment with IL-4 has been demonstrated to reduce this effect. After the stimulation of RV of 48 and 96-H, we observed a noticeable increase in the production of PDC interferon-α in normal subjects, but no asthmatic patients. The basic interferon-α expression in the PDCs and the incidence of the exacerbation of emergency asthma was higher in the 13% of patients identified as rhinovirus + than among their RV counterparts.

Conclusion: Our study discovered that the response to the stimulation of TLR-7 in the PDCs has been compromised and the durability of interferon-α expression to the stimulation of the RV has been reduced in the PDCs of asthmatic patients , which provides additional evidence of the defective innate response and the sub-specificity to RV infection in asthma. The high exacerbating history founded in VR + patients agrees with these conclusions. Additional research is needed for the modulator effect of IL-4 on the PDC stimulated by TLR-7.

Interaction between hepatitis D virus and interferon response

Chronic hepatitis (CHD) is the most serious form of viral hepatitis, rapid growth in liver-related diseases and high levels of hepatocellular carcinoma development. The causal agent, the hepatitis D virus (HDV), contains a small circular genome of the unique mounting RNA RNA (about 1.7 KB) assembling with the HDV antigen to form a complex ribonucleoprotein (RNP). HDV depends on the protein of the hepatitis B envelope (HBV) for the wrapping wrapping and novo hepatocytes; However, its replication of intracellular RNA is autonomous. In addition, HDV can amplify HBV independently by cell division.

The inevitable immune responses, mainly interferon (IFN), are crucial for controlling invasive viruses, while viruses are controlled these responses to promote their spread. Unlike VHB, HDV activates the deep IFN response through the antigen 5 (MDA5) differentiation route. This cellular response effectively removes HDV propagation mediated by cell division and, to a certain extent, the first steps of Novo HDV infection, but only slightly free the replication of RNA in hepatocytes at rest. In this review, we summarize the current knowledge of HDV structure, replication and persistence and then focus on the interaction between the HDV response and the IFN, including the activation of the IFN, the detection, the detection. Antiviral effects and viral countermeasures.

Finally, we discuss crosstalk with HBV. Treatment with anti-PD-1 immunotherapy does not lead to sustainable clinical responses in about 60% of patients with metastatic melanoma. These refractory patients, however, always respond to treatment with tumor (til) and interferon-alpha (IFNA) tumor-infiltration lymphocytes. A combination of TIL, Pegylate-Interferon-Alpha (PEG-IFNA) and Anti-PD-1 should provide safe, feasible and effective therapy in patients with metastatic melanoma, which are refractory to care treatment options.

 Impaired interferon-α expression in plasmacytoid dendritic cells in asthma
Impaired interferon-α expression in plasmacytoid dendritic cells in asthma

MPEG1 / PERFORIN-2 HAPLINUFFACEENCE Pelmicrobialic skin infections associated and considerations on interferon-γ therapy

Introduction: The gene expressed by Macrophage 1 (MPEG1) is extremely expressed in macrophages and other phagocytes. The gene code a bactericidal pores formation, brought perforine-2. Structural, animal and cellular studies have established that perforin-2 facilitates the destruction of phagocyteral microbes on its activation in acidic phasome. Compared to wild type controls, Knockout MPEG1 mice suffer significantly higher mortality rates when challenged by negative or positive gram pathogens. Only four variants of MPEG1 have been functionally functionalized, each in combination with pulmonary infections. Here we note a new variant of MPEG1 nonsense in a patient with a recently described association with persistent polymicrobial skin infections and soft tissues.

Case Description: A young adult woman was evaluated for recurring breast abscesses and cellulite and demonstrated a heterozygous and rare variant in MPEG1 p.tyr430 *. Several courses of broad spectrum antimicrobials and surgical incision and drainage have failed to solve the infection. Functional studies have revealed that the truncation variant has resulted in a considerably reduced capacity of patient’s phagocytes to kill intracellular bacteria. The patient’s derived macrophages responded to gamma interferon (IFN-γ) by considerably increasing MPEG1 expression. The IFN-γ treatment supported bactericidal activity and bactericidal healing and healing of perforin wounds.

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Conclusions: This case expands the phenotype of MPEG1 deficiency to include severe skin infection and soft tissues. We have shown that perforine-2 has reduced the bactericidal capacity of human phagocytes. Interferon-Gamma therapy increases performance of performance-2, which can compensate for such variants. Thus, treatment with IFN-γ could help prevent infections.

 

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