Topic
Antibody
About: Antibody is a research topic. Over the lifetime, 113941 publications have been published within this topic receiving 4130181 citations. The topic is also known as: Ab & antibodies.
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TL;DR: In this article , a new SARS-CoV-2 viral isolate Omicron-B.1.529 was announced, containing far more mutations in Spike (S) than previously reported variants, leading to a large number of mutations in the ACE2 binding site and rebalances receptor affinity to that of earlier pandemic viruses.
714 citations
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TL;DR: Primary, symptomatic HIV-1 infection is associated with high titers of cytopathic, replication-competent viral strains, and during such infection potential infectivity is enhanced.
Abstract: Background. Primary infection with the human immunodeficiency virus (HIV-1) frequently causes an acute, self-limited viral syndrome. To examine the relations among viral replication, the immune response of the host, and clinical illness during this initial phase of infection, we undertook a quantitative, molecular, and biologic analysis of infectious HIV-1 in the blood and plasma of three patients with symptomatic primary infection and of a sexual partner of one of them. Methods. During an eight-week period of primary infection, HIV-1 was cultured frequently in dilutions of plasma and peripheral-blood mononuclear cells (PBMC), and levels of HIV-1 antigen and antibody were determined sequentially by enzyme-linked immunosorbent assay and immunoblotting. Replication-competent HIV-1 proviruses were cloned and characterized biologically. Results. Six to 15 days after the onset of symptoms, high titers of infectious HIV-1 (from 10 to 103 tissue-culture—infective doses per milliliter of plasma) and vira...
714 citations
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TL;DR: The results suggest that further use of cA2 in MS is not warranted and that studies of other agents that antagonize TNF alpha should be carried out with frequent monitoring of gadolinium-enhanced MRIs.
Abstract: There is evidence that treatment with an antibody to tumor necrosis factor alpha (TNF alpha) improves an animal model of multiple sclerosis (MS) and is beneficial in two systemic inflammatory disease in humans, but there are no reports about anti-TNF treatment of MS. Therefore, we treated two rapidly progressive MS patients with intravenous infusions of a humanized mouse monoclonal anti-TNF antibody (cA2) in an open-label phase I safety trial and monitored their clinical status, gadolinium-enhanced brain magnetic resonance imaging (MRI), and peripheral blood and cerebrospinal fluid (CSF) immunologic status. We did not notice any clinically significant neurologic changes in either patient. The number of gadolinium-enhancing lesions increased transiently after each treatment in both patients. CSF leukocyte counts and IgG index increased after each treatment. The transient increase in the number of gadolinium-enhancing lesions that followed each infusion of cA2 together with the increase in cells and immunoglobulin in the CSF of each patient suggest that the treatment caused immune activation and an increase in disease activity. These results suggest that further use of cA2 in MS is not warranted and that studies of other agents that antagonize TNF alpha should be carried out with frequent monitoring of gadolinium-enhanced MRIs.
714 citations
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TL;DR: The results suggested that the systemic tissue damage seen in most patients with LGL leukemia and NK–type lymphoma is due to sFasL produced by these malignant cells, and neutralizing anti–FAsL antibodies or matrix metalloproteinase inhibitors may be of use in modulating such tissue damage.
Abstract: The Fas ligand (FasL), a member of the tumor necrosis factor family, induces apoptosis in Fas–bearing cells. The membrane–bound human FasL was found to be converted to a soluble form (sFasL) by the action of a matrix metalloproteinase–like enzyme. Two neutralizing monoclonal anti–human FasL antibodies were identified, and an enzyme–linked immunosorbent assay (ELISA) for sFasL in human sera was established. Sera from healthy persons did not contain a detectable level of sFasL, whereas those from patients with large granular lymphocytic (LCL) leukemia and natural killer (NK) cell lymphoma did. These malignant cells constitutively expressed FasL, whereas peripheral NK cells from healthy persons expressed FasL only on activation. These results suggested that the systemic tissue damage seen in most patients with LGL leukemia and NK–type lymphoma is due to sFasL produced by these malignant cells. Neutralizing anti–FasL antibodies or matrix metalloproteinase inhibitors may be of use in modulating such tissue damage.
713 citations
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TL;DR: Lyn-/- mice fail to mediate an allergic response to IgE cross-linking, indicating that activation of LYN plays an indispensable role in Fc epsilon RI signaling, particularly in establishing B cell tolerance.
711 citations