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Anti-Topoisomerase I Antibody

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121. Can anti-bothropstoxin-I antibodies discriminate between Bothrops jararaca and Bothrops jararacussu venoms? Full Text available with Trip Pro

Can anti-bothropstoxin-I antibodies discriminate between Bothrops jararaca and Bothrops jararacussu venoms? Snakes of the genus Bothrops, popularly known as pit vipers, are responsible for most cases of snakebite in Brazil. Within this genus, Bothrops jararacussu and B. jararaca deserve special attention due to the severity of their bites and for inhabiting densely populated areas. Regarding the treatment of snakebites by Bothrops jararacussu, questions have been raised about the effectiveness (...) studies.First, we produced a species-specific polyclonal antibody - a potential biomarker of Bothrops jararacussu venom - against bothropstoxin-I (BthTx-I), which is also found in smaller quantities in the venoms of B. jararaca from southern Brazil.Polyclonal antibodies against bothropstoxin-I could be separated into several species-specific immunoglobulins. Then, aiming to develop a system of safe and standardized immunoassay, we produced monoclonal antibodies. Seven hybridomas were obtained. Five of them

2017 The journal of venomous animals and toxins including tropical diseases

122. Phase I trial and pharmacokinetic study of tanibirumab, a fully human monoclonal antibody to vascular endothelial growth factor receptor 2, in patients with refractory solid tumors Full Text available with Trip Pro

Phase I trial and pharmacokinetic study of tanibirumab, a fully human monoclonal antibody to vascular endothelial growth factor receptor 2, in patients with refractory solid tumors Background Tanibirumab is a fully human monoclonal antibody to vascular endothelial growth factor receptor 2 (VEGFR-2). We conducted a first-in-human phase I study of tanibirumab in patients with solid tumors refractory to standard chemotherapy. Primary endpoints were evaluating safety, pharmacokinetics (PKs

2017 Investigational new drugs

123. Type I interferon signaling is required for the APOBEC3/Rfv3-dependent neutralizing antibody response but not innate retrovirus restriction Full Text available with Trip Pro

Type I interferon signaling is required for the APOBEC3/Rfv3-dependent neutralizing antibody response but not innate retrovirus restriction APOBEC3/Rfv3 restricts acute Friend retrovirus (FV) infection and promotes virus-specific neutralizing antibody (NAb) responses. Classical Rfv3 studies utilized FV stocks containing lactate-dehydrogenase elevating virus (LDV), a potent type I interferon inducer. Previously, we showed that APOBEC3 is required for the anti-FV activity of exogenous IFN-alpha (...) treatment. Thus, type I interferon receptor (IFNAR) signaling may be required for the APOBEC3/Rfv3 response.To test if the APOBEC3/Rfv3 response is dependent on type I IFN signaling, we infected IFNAR knockout versus IFNAR/APOBEC3 double-knockout mice with FV/LDV or LDV-free FV, and evaluated acute FV infection and subsequent NAb titers. We show that LDV co-infection and type I IFN signaling are not required for innate APOBEC3-mediated restriction. By contrast, removal of LDV and/or type I IFN signaling

2017 Retrovirology

124. HIV-antibody complexes enhance production of type I interferon by plasmacytoid dendritic cells Full Text available with Trip Pro

HIV-antibody complexes enhance production of type I interferon by plasmacytoid dendritic cells Type I IFN production is essential for innate control of acute viral infection; however, prolonged high-level IFN production is associated with chronic immune activation in HIV-infected individuals. Although plasmacytoid DCs (pDCs) are a primary source of IFN, the mechanisms that regulate IFN levels following the acute phase are unknown. We hypothesized that HIV-specific Ab responses regulate late IFN

2017 The Journal of clinical investigation

125. Glomerulocapillary miRNA response to HLA-class I antibody in vitro and in vivo Full Text available with Trip Pro

Glomerulocapillary miRNA response to HLA-class I antibody in vitro and in vivo Changes in miRNA expression glomerular of capillaries during antibody-mediated rejection (ABMR) are poorly understood and could contribute to the deleterious inflammation and fibrosis of ABMR via suppression of target genes. A better understanding could lead to novel diagnostic tools and reveal novel therapeutic targets. We explored deregulated miRNAs in an glomeruloendothelial in vitro model of ABMR due to class I (...) ) and 2 downregulated (miR29b-3p, miR-885-5p) in DSA+ vs.A random forest analysis based on glomerular miRNAs identified 18/20 DSA+ and 8/10 controls correctly. This glomerulocapillary miRNA signature associated with HLA class I-DSA could improve our understanding of ABMR and be useful for diagnostic or therapeutic purposes.

2017 Scientific reports

126. Phase I Study of Anti-GM2 Ganglioside Monoclonal Antibody BIW-8962 as Monotherapy in Patients with Previously Treated Multiple Myeloma Full Text available with Trip Pro

Phase I Study of Anti-GM2 Ganglioside Monoclonal Antibody BIW-8962 as Monotherapy in Patients with Previously Treated Multiple Myeloma BIW-8962 is a monoclonal antibody to GM2 ganglioside that shows preclinical activity towards multiple myeloma (MM) cell lines and in animal models bearing MM xenografts. The objective of this study was to determine the safety, tolerability, maximum tolerated dose (MTD), pharmacokinetics, potential immunogenicity, and preliminary clinical efficacy of BIW-8962

2016 Oncology and therapy

127. Upregulation of HLA Class I Expression on Tumor Cells by the Anti-EGFR Antibody Nimotuzumab Full Text available with Trip Pro

Upregulation of HLA Class I Expression on Tumor Cells by the Anti-EGFR Antibody Nimotuzumab Defining how epidermal growth factor receptor (EGFR)-targeting therapies influence the immune response is essential to increase their clinical efficacy. A growing emphasis is being placed on immune regulator genes that govern tumor - T cell interactions. Previous studies showed an increase in HLA class I cell surface expression in tumor cell lines treated with anti-EGFR agents. In particular, earlier (...) studies of the anti-EGFR blocking antibody cetuximab, have suggested that increased tumor expression of HLA class I is associated with positive clinical response. We investigated the effect of another commercially available anti-EGFR antibody nimotuzumab on HLA class I expression in tumor cell lines. We observed, for the first time, that nimotuzumab increases HLA class I expression and its effect is associated with a coordinated increase in mRNA levels of the principal antigen processing

2017 Frontiers in pharmacology

128. Immunochemical Approach for Monitoring of Structural Transition of ApoA-I upon HDL Formation Using Novel Monoclonal Antibodies Full Text available with Trip Pro

Immunochemical Approach for Monitoring of Structural Transition of ApoA-I upon HDL Formation Using Novel Monoclonal Antibodies Apolipoprotein A-I (apoA-I) undergoes a large conformational reorganization during remodeling of high-density lipoprotein (HDL) particles. To detect structural transition of apoA-I upon HDL formation, we developed novel monoclonal antibodies (mAbs). Splenocytes from BALB/c mice immunized with a recombinant human apoA-I, with or without conjugation with keyhole limpet (...) hemocyanin, were fused with P3/NS1/1-Ag4-1 myeloma cells. After the HAT-selection and cloning, we established nine hybridoma clones secreting anti-apoA-I mAbs in which four mAbs recognize epitopes on the N-terminal half of apoA-I while the other five mAbs recognize the central region. ELISA and bio-layer interferometry measurements demonstrated that mAbs whose epitopes are within residues 1-43 or 44-65 obviously discriminate discoidal and spherical reconstituted HDL particles despite their great

2017 Scientific reports

129. A therapeutic T cell receptor mimic antibody targets tumor-associated PRAME peptide/HLA-I antigens Full Text available with Trip Pro

A therapeutic T cell receptor mimic antibody targets tumor-associated PRAME peptide/HLA-I antigens Preferentially expressed antigen in melanoma (PRAME) is a cancer-testis antigen that is expressed in many cancers and leukemias. In healthy tissue, PRAME expression is limited to the testes and ovaries, making it a highly attractive cancer target. PRAME is an intracellular protein that cannot currently be drugged. After proteasomal processing, the PRAME300-309 peptide ALYVDSLFFL (ALY) is presented (...) in the context of human leukocyte antigen HLA-A*02:01 molecules for recognition by the T cell receptor (TCR) of cytotoxic T cells. Here, we have described Pr20, a TCR mimic (TCRm) human IgG1 antibody that recognizes the cell-surface ALY peptide/HLA-A2 complex. Pr20 is an immunological tool and potential therapeutic agent. Pr20 bound to PRAME+HLA-A2+ cancers. An afucosylated Fc form (Pr20M) directed antibody-dependent cellular cytotoxicity against PRAME+HLA-A2+ leukemia cells and was therapeutically effective

2017 The Journal of clinical investigation

130. Phase I trial of anti-GD2 monoclonal antibody hu3F8 plus GM-CSF: Impact of body weight, immunogenicity and anti-GD2 response on pharmacokinetics and survival Full Text available with Trip Pro

Phase I trial of anti-GD2 monoclonal antibody hu3F8 plus GM-CSF: Impact of body weight, immunogenicity and anti-GD2 response on pharmacokinetics and survival Fifty-seven stage 4 patients with refractory/relapsed neuroblastoma were enrolled in a phase I trial (Clinicaltrials.gov NCT01757626) using humanized anti-GD2 monoclonal antibody hu3F8 in combination with granulocyte-macrophage colony-stimulating factor. The influence of body weight and human anti-human antibody (HAHA (...) and overall survival was estimated by the Kaplan-Meier method. Despite dosing being based on body weight, smaller patients had consistently lower area-under-the-curve and faster clearance over the 15 dose levels (0.9 to 9.6 mg/kg per treatment cycle) in this trial. Positive HAHA, defined by the upper limit of normal, when measured within 10 days from the last hu3F8 dose received, was associated with significantly lower serum hu3F8. Despite prior sensitization to other anti-GD2 antibody, e.g. mouse 3F8

2017 Oncoimmunology

131. Neuropathogenesis of Zika Virus in a Highly Susceptible Immunocompetent Mouse Model after Antibody Blockade of Type I Interferon Full Text available with Trip Pro

Neuropathogenesis of Zika Virus in a Highly Susceptible Immunocompetent Mouse Model after Antibody Blockade of Type I Interferon Animal models are needed to better understand the pathogenic mechanisms of Zika virus (ZIKV) and to evaluate candidate medical countermeasures. Adult mice infected with ZIKV develop a transient viremia, but do not demonstrate signs of morbidity or mortality. Mice deficient in type I or a combination of type I and type II interferon (IFN) responses are highly (...) susceptible to ZIKV infection; however, the absence of a competent immune system limits their usefulness for studying medical countermeasures. Here we employ a murine model for ZIKV using wild-type C57BL/6 mice treated with an antibody to disrupt type I IFN signaling to study ZIKV pathogenesis. We observed 40% mortality in antibody treated mice exposed to ZIKV subcutaneously whereas mice exposed by intraperitoneal inoculation were highly susceptible incurring 100% mortality. Mice infected by both exposure

2017 PLoS neglected tropical diseases

132. Influence of type I IFN signaling on anti-MOG antibody-mediated demyelination Full Text available with Trip Pro

Influence of type I IFN signaling on anti-MOG antibody-mediated demyelination Antibodies with specificity for myelin oligodendrocyte glycoprotein (MOG) are implicated in multiple sclerosis and related diseases. The pathogenic importance of anti-MOG antibody in primary demyelinating pathology remains poorly characterized.The objective of this study is to investigate whether administration of anti-MOG antibody would be sufficient for demyelination and to determine if type I interferon (IFN (...) ) signaling plays a similar role in anti-MOG antibody-mediated pathology, as has been shown for neuromyelitis optica-like pathology.Purified IgG2a monoclonal anti-MOG antibody and mouse complement were stereotactically injected into the corpus callosum of wild-type and type I IFN receptor deficient mice (IFNAR1-KO) with and without pre-established experimental autoimmune encephalomyelitis (EAE).Anti-MOG induced complement-dependent demyelination in the corpus callosum of wild-type mice and did not occur

2017 Journal of neuroinflammation

133. Interferon α kinoid induces neutralizing anti-interferon α antibodies that decrease the expression of interferon-induced and B cell activation associated transcripts: analysis of extended follow-up data from the interferon α kinoid phase I/II study. Full Text available with Trip Pro

Interferon α kinoid induces neutralizing anti-interferon α antibodies that decrease the expression of interferon-induced and B cell activation associated transcripts: analysis of extended follow-up data from the interferon α kinoid phase I/II study. IFN α Kinoid (IFN-K) is a therapeutic vaccine composed of IFNα2b coupled to a carrier protein. In a phase I/II placebo-controlled trial, we observed that IFN-K significantly decreases the IFN gene signature in whole blood RNA samples from SLE (...) patients. Here, we analysed extended follow-up data from IFN-K-treated patients, in order to evaluate persistence of neutralizing anti-IFNα Abs antibodies (Abs), and gene expression profiling.Serum and whole blood RNA samples were obtained in IFN-K-treated patients included in the follow-up study, in order to determine binding and neutralizing anti-IFNα Ab titres, and perform high-throughput transcriptomic studies.Neutralization studies of 13 IFNα subtypes demonstrated the polyclonal nature of the Ab

2017 Rheumatology (Oxford, England) Controlled trial quality: uncertain

134. IFN-α augments NK-mediated antibody-dependent cellular cytotoxicity (ADCC) of HIV-1 infected autologous CD4+ T cells regardless of MHC-I downregulation. Full Text available with Trip Pro

IFN-α augments NK-mediated antibody-dependent cellular cytotoxicity (ADCC) of HIV-1 infected autologous CD4+ T cells regardless of MHC-I downregulation.

2017 AIDS

135. <b>Therapy of Small-cell Lung Cancer (SCLC) With a Topoisomerase-I-inhibiting Antibody-Drug Conjugate (ADC) Targeting Trop-2, Sacituzumab Govitecan</b>. Full Text available with Trip Pro

Therapy of Small-cell Lung Cancer (SCLC) With a Topoisomerase-I-inhibiting Antibody-Drug Conjugate (ADC) Targeting Trop-2, Sacituzumab Govitecan. Purpose: We evaluated a Trop-2-targeting antibody conjugated with SN-38 in metastatic small cell lung cancer (mSCLC) patients.Experimental Design: Sacituzumab govitecan was studied in patients with pretreated (median, 2; range, 1-7) mSCLC who received either 8 or 10 mg/kg i.v. on days 1 and 8 of 21-day cycles. The primary endpoints were safety (...) . No antibodies to the drug conjugate or its components were detected on serial blood collections.Conclusions: Sacituzumab govitecan appears to have a safe and effective therapeutic profile in heavily pretreated mSCLC patients, including those who are chemosensitive or chemoresistant to first-line chemotherapy. Additional studies as a monotherapy or combination therapy are warranted. Clin Cancer Res; 23(19); 5711-9. ©2017 AACR.©2017 American Association for Cancer Research.

2017 Clinical Cancer Research

136. Altered β<sub>2</sub> glycoprotein-I expression on microparticles in the presence of antiphospholipid antibodies. Full Text available with Trip Pro

Altered β2 glycoprotein-I expression on microparticles in the presence of antiphospholipid antibodies. Essentials β2 glycoprotein-I (β2 GPI) is a scavenger molecule that binds to microparticles (MPs). β2 GPI expression on MPs was measured in systemic lupus erythematosus (SLE) patients and controls. β2 GPI positive MPs is depressed among SLE patients positive for antiphospholipid antibodies. Complex formation between β2 GPI on MPs and patients own anti-β2 GPI may disturb MP clearance (...) . Click to hear an ISTH Academy presentation on antiphospholipid antibody syndrome by Drs de Laat and Bertolaccini SUMMARY: Background Antiphospholipid antibodies (aPLs) together with thrombosis and/or pregnancy morbidities characterize the antiphospholipid syndrome. β2 -Glycoprotein I (β2 GPI), the most important antigen for aPLs, is a scavenger molecule that specifically binds to phosphatidylserine (PS) expressed on microparticles (MPs). Objectives To evaluate β2 GPI-expressing MPs in patients

2017 Journal of Thrombosis and Haemostasis

137. Phase I randomized study of KHK4083, an anti-OX40 monoclonal antibody, in patients with mild to moderate plaque psoriasis. Full Text available with Trip Pro

Phase I randomized study of KHK4083, an anti-OX40 monoclonal antibody, in patients with mild to moderate plaque psoriasis. OX40 (CD134) is expressed in lesional but not healthy skin of patients with psoriasis. KHK4083 is a fully human monoclonal antibody against OX40.The primary aim of this first-in-human phase 1 study was to determine the safety and tolerability of ascending single doses of KHK4083 in patients with mild to moderate plaque psoriasis. Secondary aims were to determine (...) , and 1.0 mg/kg SC.There were no severe or serious adverse events (AEs), or discontinuations because of AEs. The most frequent treatment-related AEs in the 55 patients who received KHK4083 were mild or moderate chills (9.1%), and infusion/injection site reactions (7.3%). No clinically meaningful or dose-related changes from baseline in laboratory values, vital signs, ECG recordings or physical examinations were observed. Some KHK4083 recipients (10/54) developed anti-KHK4083 antibodies following

2017 Journal of the European Academy of Dermatology and Venereology Controlled trial quality: predicted high

138. Immune Complexes of Beta-2-Glicoprotein I Bounded to IgA: A Novel Marker Able to Predict Thrombosis After Renal Transplantation in Patients with Antiphospholipid Antibodies. Full Text available with Trip Pro

Immune Complexes of Beta-2-Glicoprotein I Bounded to IgA: A Novel Marker Able to Predict Thrombosis After Renal Transplantation in Patients with Antiphospholipid Antibodies.

2017 Circulation

139. Addition of azathioprine to the switch of anti-TNF in patients with IBD in clinical relapse with undetectable anti-TNF trough levels and antidrug antibodies: a prospective randomised trial

Addition of azathioprine to the switch of anti-TNF in patients with IBD in clinical relapse with undetectable anti-TNF trough levels and antidrug antibodies: a prospective randomised trial Addition of Azathioprine to the Switch of anti-TNF in Patients With IBD in Clinical Relapse With Undetectable anti-TNF Trough Levels and Antidrug Antibodies: A Prospective Randomised Trial - PubMed This site needs JavaScript to work properly. Please enable it to take advantage of the complete set of features (...) : Send even when there aren't any new results Optional text in email: Save Cancel Create a file for external citation management software Create file Cancel Actions Cite Share Permalink Copy Page navigation Gut Actions . 2020 Jan 24;gutjnl-2019-319758. doi: 10.1136/gutjnl-2019-319758. Online ahead of print. Addition of Azathioprine to the Switch of anti-TNF in Patients With IBD in Clinical Relapse With Undetectable anti-TNF Trough Levels and Antidrug Antibodies: A Prospective Randomised Trial

2020 EvidenceUpdates

140. Soft tissue infection with decreased pneumococcal antibody response

with decreased pneumococcal antibody response Q: 1/5/2020 I have a question about specific antibody deficiency. I have a patient who is a 36 year-old female referred for immunodeficiency evaluation by PCP. This year she had a C-section that resulted in an infected wound. She also had three episodes of mastitis, and each episode was treated with antibiotics. Recently she had a left jaw lump, in which she saw ENT and they were unclear on what it was and sent the patient for CT of jaw and started the patient (...) mastitis is not generally seen in specific antibody deficiency, would the diagnosis of specific antibody deficiency be appropriate in this patient? Would she be an increased risk of sinopulmonary infections in the future due to poor response to Pneumovax? Should she receive Prevnar? I appreciate any guidance. A: I do not favor a diagnosis of specific antibody deficiency with these laboratory data and clinical presentation. The interpretation of polysaccharide antibody response is complicated without

2020 American Academy of Allergy, Asthma & Immunology - Ask the Expert

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