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Interferon β associated nephropathy in a Multiple Sclerosis patient: A case and review.

BACKGROUND: Interferon beta (IFN β) subtypes are largely used as immunomodulatory agents in Multiple Sclerosis (MS) treatment. While being generally well tolerated, they can cause various side effects. Adverse effects related to kidney are rarely reported. CASE REPORT: We report a 32 years old male patient who developed nephrotic syndrome while receiving IFN β for MS. Biopsy showed focal segmental glomerulosclerosis. He went into remisson after cessation of drug and with the aid of angiotensin II antagonists. Here, we report this case and a review of similar cases reported in literature. CON

Rescue of a recombinant Machupo virus from cloned cDNAs and in vivo characterization in interferon (αβ/γ) receptor double knockout mice.

Machupo virus (MACV) is the etiological agent of Bolivian hemorrhagic fever (BHF), a reemerging and neglected tropical disease associated with high mortality. The prototypical strain of MACV, Carvallo, was isolated from a human patient in 1963, but minimal in vitro and in vivo characterization has been reported. To this end, we utilized reverse genetics to rescue a pathogenic MACV from cloned cDNAs. The recombinant MACV (rMACV) had in vitro growth properties similar to those of the parental MACV. Both viruses caused similar disease development in alpha/beta and gamma interferon receptor knocko

Neuroprotective Strategies after Neonatal Hypoxic Ischemic Encephalopathy.

Neonatal hypoxic ischemic encephalopathy (HIE) is a devastating disease that primarily causes neuronal and white matter injury and is among … europrotective molecules that bring hope to future treatments such as melatonin, topiramate, xenon, interferon-beta, stem cell transplantation. This review will also discuss some of the most recent trials being conducted in the clinical setting and evaluate what directions are needed in the future.

Listeria monocytogenes infection induces prosurvival metabolic signaling in macrophages.

Host cells use metabolic signaling through the LXRα nuclear receptor to defend against Listeria monocytogenes infection. 25-Hydroxycholesterol is a natural ligand of LXRs that is produced by the enzyme cholesterol 25-hydroxylase (CH25H). We found that expression of Ch25h is upregulated following L. monocytogenes infection in a beta interferon (IFN-β)-dependent fashion. Moreover, increased Ch25h expression promotes survival of L. monocytogenes-infected cells and increases sensitivity of the host to infection. We determined that expression of Cd5l, a prosurvival gene, is controlled by CH25H. In

Прогрессивная многофукальная лейкоэнцефалопатия, напоминающая центральную нервную систему системная волчанка эритематос.

21-летняя женщина с 6-летней историей SLE с нарушениями речи и неуклюжестью правой руки, а также проявлениями активной болезни, что говорит о центральной нервной системе SLE. Несмотря на агрессивное лечение SLE, ее неврологическое состояние ухудшилось. МРТ продемонстрировала низкую интенсивность в изображениях, взвешенных по Т1, и высокую интенсивность в изображениях, взвешенных по Т2 в белом материи двустороннего церебрального и мозжечного мозга, совместимых с прогрессивной многофукальной лейкоэнцефалопатией (ПМЛ). Внутреннее управление интерферон-бетой, казалось, замедлило ухудшение ее МРТ и

Совпадение в аннотации оригинала
A 21-year-old woman with a 6-year history of SLE presented with a speech disturbance and right hand clumsiness along with manifestations of … um, compatible with progressive multifocal leukoencephalopathy (PML). Intraspinal administration of interferon-beta seemed to slow the deterioration of her MRI and neurological findings. However, she eventually developed decerebrate rigidity and died due to candidemia. DNA of the JC virus was detected in the autopsied brain by the polymerase chain reaction techni …

[Acute congenital monoblastic leukemia and 9;11 translocation: a case].

Acute leukemia in the newborn child is a rare event. The clinical and biological characteristics differ from those normally encountered in the older child. Tumoral syndrome and extra-medullar locations are frequently described in the literature. Many authors have noted the difficulty of diagnosis due to the immaturity of the malignant proliferation. While it is generally agreed that therapeutic abstention is justified in the leukemoid reaction in Down's syndrome, the choice is debatable in the phenotypically intact newborn. For this reason, blastic karyotype analysis is essential and may provi

Mechanisms of interferon-induced inhibition of Toxoplasma gondii replication in human retinal pigment epithelial cells.

Inflammation associated with retinochoroiditis is a major complication of ocular toxoplasmosis in infants and immunocompetent individuals. Moreover, Toxoplasma gondii-induced retinal disease causes serious complications in patients with AIDS and transplant patients. The retinal pigment epithelial (RPE) cell is an important regulatory cell within the retina and is one of the cells infected with T. gondii in in vivo. We have developed a human RPE (HRPE) cell in vitro model system to evaluate T. gondii replication and the regulation of this replication by cytokines. T. gondii replication was quan

Age-dependent expression and antiviral activity of interferon epsilon in respiratory epithelium.

UNLABELLED: Respiratory syncytial virus (RSV) disease burden is greatest between 6 weeks and 6 months of life, with young age the most common risk factor among hospitalized children. A robust innate immune response in the airway epithelium is crucial for mitigating RSV-associated disease, but early-life immune responses to infection remain largely unexplored. RNA-seq analysis of RSV-infected primary nasal epithelial cell cultures from healthy infants at birth and 1 year revealed diminished expression of interferon epsilon (IFNE), a poorly characterized type I IFN, in newborns vs 1 year. We hyp

STING agonists drive recruitment and intrinsic type I interferon responses in monocytic lineage cells for optimal anti-tumor immunity.

The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway, a sensor of cytosolic DNA, orchestrates the production of proinflammatory cytokines, chemokines, and type I interferons (IFN-Is), thereby contributing to spontaneous tumor surveillance. Intratumoral delivery of synthetic STING agonists induces IFN-I-dependent tumor regression in preclinical cancer models and is being tested clinically. In this study, we investigate the role of monocytic lineage cells (MCs) in response to STING agonist induced IFN-I signaling. We show that CCR2-deficient mice, lacking inflammatory

Regulation of STAT1 and STAT4 Expression by Growth Factor and Interferon Supplementation in Sjögren's Syndrome Cell Culture Models.

Our goal was to investigate the effects of epidermal growth factor (EGF) and interferons (IFNs) on signal transducer and activator of transcription STAT1 and STAT4 mRNA and active phosphorylated protein expression in Sjögren's syndrome cell culture models. iSGECs (immortalized salivary gland epithelial cells) and A253 cells were treated with EGF, IFN-alpha, -beta, -gamma, or mitogen-activated protein kinase p38 alpha (p38-MAPK) inhibitor for 0-24-48-72 h. STAT1 and STAT4 mRNA expression was quantified by qRT-PCR. Untreated and treated cells were compared using the delta-delta-CT method based o

In-Depth, Label-Free Analysis of the Erythrocyte Cytoplasmic Proteome in Diamond Blackfan Anemia Identifies a Unique Inflammatory Signature.

Diamond Blackfan Anemia (DBA) is a rare, congenital erythrocyte aplasia that is usually caused by haploinsufficiency of ribosomal proteins due to diverse mutations in one of several ribosomal genes. A striking feature of this disease is that a range of different mutations in ribosomal proteins results in similar disease phenotypes primarily characterized by erythrocyte abnormalities and macrocytic anemia, while most other cell types in the body are minimally affected. Previously, we analyzed the erythrocyte membrane proteomes of several DBA patients and identified several proteins that are not

Characterization of the interferon-producing cell in mice infected with Listeria monocytogenes.

Production of type I interferons (IFN-I, mainly IFNalpha and IFNbeta) is a hallmark of innate immune responses to all classes of pathogens. When viral infection spreads to lymphoid organs, the majority of systemic IFN-I is produced by a specialized "interferon-producing cell" (IPC) that has been shown to belong to the lineage of plasmacytoid dendritic cells (pDC). It is unclear whether production of systemic IFN-I is generally attributable to pDC irrespective of the nature of the infecting pathogen. We have addressed this question by studying infections of mice with the intracellular bacterium

Azithromycin enhances epithelial antiviral immunity in uncontrolled asthma: results from the AZIMUNE randomised controlled trial.

BACKGROUND: Viral respiratory infections are the leading trigger of asthma exacerbations, and impaired epithelial type I and III interferon (IFN) responses may contribute to more severe exacerbations. Azithromycin reduces exacerbations clinically, but its effects on epithelial antiviral immunity remain unclear. This study investigated whether azithromycin treatment enhances airway epithelial antiviral responses and modulates alarmin concentrations in patients with uncontrolled asthma. METHODS: In the investigator-initiated, double-blind, placebo-controlled AZIMUNE trial, 40 adults with uncont

Interferon-epsilon, an estrogen-induced type I interferon, is uniquely exploited by Neisseria gonorrhoeae via effects on sialic acid metabolism.

The female genital mucosa expresses the hormone-dependent type I interferon (IFN), IFN-epsilon (IFN-ε), which protects against chlamydia and herpes infection. Surprisingly, we found that IFN-ε knockout (Ifnε-/-) mice and type I IFN receptor knockout (Ifnar1-/-) mice exhibited enhanced clearance of Neisseria gonorrhoeae (Ng). This result was phenocopied using blocking anti-IFNAR monoclonal antibody (mAb). Ng colonization of the Ifnε-/- urogenital tract was restored by exogenous recombinant IFN-ε or IFN-β. Clearance of Ng in anti-IFNAR-treated mice required the expression of the cathelicidin mCR

Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositis.

OBJECTIVES: To determine whether type 1 interferon (IFN) proteins in blood are associated with downstream type 1 IFN-inducible gene expression in blood from patients with myositis. METHODS: IFNα, IFNβ and IFNω concentrations were measured by ELISA in 129 blood samples (from 93 patients with dermatomyositis (DM), inclusion body myositis, polymyositis and other muscle diseases and from 36 healthy volunteers). Their concentrations were correlated with their ability to stimulate type 1 IFN-inducible gene transcription in a functional assay for 123 of these samples and the type 1 IFN-inducible blo

Dose-dependent activation of the Hippo pathway by Type I and Type III interferons suppresses tissue repair by human bronchial epithelial cells.

Interferons (IFNs) are potent antiviral cytokines that are rapidly activated when infected cells sense a virus, but continued IFN production following acute infection is linked to impaired recovery. IFNs protect against infection by inducing a suite of antiviral effectors in IFN receptor-expressing cells via JAK/STAT signaling. However, how IFNs curtail tissue repair is not fully understood. Here, we studied the effects of Type III IFNs (IFNλ1 and IFNλ2) and Type I IFN (IFNβ) on tissue repair functions of human bronchial epithelial cells (HBEC). We show that both Type III IFNs and IFNβ reduce

HERC5 E3 ligase mediates ISGylation of hepatitis B virus X protein to promote viral replication.

Ubiquitin and ubiquitin-like protein modification play important roles in modulating the functions of viral proteins in many viruses. Here we demonstrate that hepatitis B virus (HBV) X protein (HBx) is modified by ISG15, which is a type I IFN-inducible, ubiquitin-like protein; this modification is called ISGylation. Immunoblot analyses revealed that HBx proteins derived from four different HBV genotypes accepted ISGylation in cultured cells. Site-directed mutagenesis revealed that three lysine residues (K91, K95 and K140) on the HBx protein, which are well conserved among all the HBV genotypes

USP26 suppresses type I interferon signaling by targeting TRAF3 for deubiquitination.

Deubiquitinating enzymes (DUBs) play a pivotal role in regulating the antiviral immune response by targeting members of the RLR signaling pathway. As a pivotal member of the RLR pathway, TRAF3 is essential for activating the MAVS/TBK-1/IRF3 signaling pathway in response to viral infection. Despite its importance, the function of DUBs in the TRAF3-mediated antiviral response is poorly understood. Ubiquitin-specific protease 26 (USP26) regulates the RLR signaling pathway to modulate the antiviral immune response. The results demonstrate that EV71 infection upregulates the expression of USP26. Kn

Type I interferon shapes brain distribution and tropism of tick-borne flavivirus.

Viral tropism within the brain and the role(s) of vertebrate immune response to neurotropic flaviviruses infection is largely understudied. We combine multimodal imaging (cm-nm scale) with single nuclei RNA-sequencing to study Langat virus in wildtype and interferon alpha/beta receptor knockout (Ifnar-/-) mice to visualize viral pathogenesis and define molecular mechanisms. Whole brain viral infection is imaged by Optical Projection Tomography coregistered to ex vivo MRI. Infection is limited to grey matter of sensory systems in wildtype mice, but extends into white matter, meninges and choroi