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The Severe Combined Immunodeficiency (scid) Mutation, Chromosome 16
Published in John P. Sundberg, Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
John P. Sundberg, Leonard D. Shultz
Severe combined immunodeficiency (scid) mice have been found to lack functional T and B cells, as well as Thy-l+ dendritic epidermal cells, but they exhibit normal differentiation and function of myeloid cells, antigen-presenting cells, and natural killer cells.8–13 This mutation appears to cause an abnormal recombinase system for the assemblage of antigen receptor genes in developing lymphocytes.10 The defect appears to be restricted to the level of the lymphopoietic stem cell. While the majority of scid/scid mice lack functional lymphoid cells, approximately 15% of scid/scid mice express detectable serum Ig. These so-called “leaky” scid/scid mice also express functional T cells.14
Immunoglobulins
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Many of the molecules participating in the rearrangement process have yet to be identified. Two candidates for components of a “recombinase complex” are the products of the recombinase activation genes: RAG-1 and RAG-2. Recombinase activity is an integral part of the regulation of B cell development. RAG products are prominent in young lymphocytes which are actively rearranging their Ig genes. RAG activity disappears in mature lymphocytes. Fibroblasts do not normally rearrange Ig gene segments. However, when RAG genes are introduced into these cells, they acquire the capacity for Ig gene rearrangement. It is not clear whether these genes encode recombinase components with enzymatic and/or DNA-binding activity, or if they are transcriptional regulators of genes encoding the actual recombinases.
Practical Approach to Molecular Biology in Hematopathology
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Anwar Mikhael, Harold R. Schumacher
Assembly of both heavy- and light-chain genes involves similar molecular mechanisms. Present at the boundaries of all germline segments are consensus sequences consisting of a conserved palindromic heptamer and nanomer separated by either 12 or 23 bp of non-conserved spacer sequences. Recombination is catalysed by the recombinase (RAG-1 and RAG-2) system. In addition, terminal deoxynucleotidyl transferase (TdT) will add a few nucleotides at the junction, thereby inducing more Ig diversity (1,2).
An insight into clinical and laboratory detections for screening and diagnosis of cervical cancer
Published in Expert Review of Molecular Diagnostics, 2023
Shruthi Padavu, Pooja Aichpure, Ballamoole Krishna Kumar, Anoop Kumar, RadhaKanta Ratho, Shipra Sonkusare, Indrani Karunasagar, Iddya Karunasagar, Praveen Rai
The recombinase polymerase amplification (RPA) has evolved as a novel isothermal amplification technique for the molecular diagnosis of HR-HPV. The RPA, unlike many other isothermal methods, does not require high temperatures and proceeds in the range of 37–42°C within 20–30 minutes [75]. This technique employs the recombinase activity and strand-displacing activity of the enzyme to unwind dsDNA and amplify the target DNA, respectively. The RPA technique is quite helpful in detecting HR-HPV because of its rapidity and near-normal reaction temperature. The end-point of the isothermal amplification product can be interpreted using fluorescent-based nucleic acid detection or gel electrophoresis. End-point detection can also be achieved by chemically labeling the RPA reaction and using lateral flow strips that enable instrument-free signal readouts. TwistAmp® (TwistDx™, UK) offers a variety of RPA kits with varying end-point detection for research and commercial applications [76]. The RPA achieves exponential amplification without the necessity for the pretreatment of the DNA sample. The RPA assay was shown to be a powerful approach for detecting HPV and may be a beneficial tool for the early diagnosis of HPV infection in prognostic applications [77].
Recent progress and challenges in drug development to fight hand, foot and mouth disease
Published in Expert Opinion on Drug Discovery, 2020
Ze Qin Lim, Qing Yong Ng, Justin Wei Qing Ng, Vikneswari Mahendran, Sylvie Alonso
Validation-based insertional mutagenesis (VBIM) is a novel function-based, forward genetic screening method that involves the insertion of a reversible promoter. EV-A71 is a lytic virus, and infected cells typically exhibit massive CPE. Mutations that either silence proviral host factors or drive the expression of antiviral factors are expected to protect the infected cells from undergoing CPE. In addition, the mutant phenotype can be reversed through Cre recombinase-mediated removal of the insert, thereby validating the role of the target gene in the phenotype observed [133]. This approach can be applied to a wide range of mammalian cell lines that can generate high titers of VBIM lentivirus. Using this technique, Nup214 was reported to play an important role during EV-A71 replication [134]. In a separate study using VBIM, KREMEN1 was identified as a novel host receptor for CV-A10 and enteroviruses-A [135]. KREMEN1 is a transmembrane molecule that regulates WNT signaling and promotes the uptake of viral-receptor complexes through clathrin-mediated endocytosis [136,137]. KREMEN1 and KREMEN2-deficient mice remained asymptomatic upon infection with CV-A10, with absence of viral replication in the muscle tissues [135].
An overview of human leptospirosis vaccine design and future perspectives
Published in Expert Opinion on Drug Discovery, 2020
Carolina R. Felix, Bianca S. Siedler, Liana N. Barbosa, Gabriana R. Timm, Johnjoe McFadden, Alan J. A. McBride
Surprisingly, cytosolic proteins have also been shown to elicit protective immunity even though they are not the logical choice for vaccine candidates as they are not generally thought to be expressed on the bacterial surface. Recently, recombinase A (RecA), a cytosolic protein, protected 83% of immunized animals against homologous and heterologous challenges and induced sterilizing immunity [44]. Although several antigens have elicited sterilizing immunity (Table 1), this is not generally considered a priority for a leptospiral vaccine since person-to-person transmission of leptospirosis is not considered to be a risk [27]. As the search for novel protective candidates is limited by several logistical constraints, including the indispensable use of experimental animals and funding, the field has tended to focus on OMPs, as these are more likely to elicit protective immunity than cytosolic proteins.