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Rise of the Microbial World: An Economic Point of View
Published in Jyoti Ranjan Rout, Rout George Kerry, Abinash Dutta, Biotechnological Advances for Microbiology, Molecular Biology, and Nanotechnology, 2022
Microbes are extensively studied for vaccine production. Vaccines are introduced in the body as suspensions of an avirulent form of a pathogen that can be live-attenuated or used as toxoids for inducing a specific and adaptive immune response in the host against a number of diseases. When the vaccine carrying an epitope similar to that of the antigen present on the surface of the disease-causing microbe enters the body, it triggers the host immune response by the generation of antigen-specific antibodies. Subsequently, upon exposure to the disease-causing microbe, the immune system identifies the antigen and responds rapidly to it by producing the same antibodies made against the vaccine and thereby preventing the development of the disease (Lee et al., 2012). The first vaccine discovery dates back to 1796 by British physician Edward Jenner who used cowpox virus, vaccinia like lesions on a milkmaid’s hand to prevent infection against the smallpox virus (Riedel, 2005). Further research resulted in the discovery of a series of vaccines against mumps, measles, plague, rabies, polio, typhoid fever, cholera, tetanus, tuberculosis, and others.
Evidence for a Role of Infections in the Activation of Autoreactive T Cells and the Pathogenesis of Autoimmunity
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
J. Ludovic Croxford, Stephen D. Miller
Epitope spreading (Fig. 1B) describes a mechanism by which autoimmunity is initiated via the de novo activation of autoreactive T cells, subsequent to self-tissue damage following infection.9 Damage may occur directly, via virus-mediated tissue destruction or indirectly, as a result of virus-specific T cell immune responses. Following tissue destruction, self-peptides may be processed by activated host APC in the infected organ and presented to autoreactive CD4+ T cells, which can initiate the autoimmune response. In addition, multiple self-tissue specificities may arise with time leading to a further progression of autoimmune disease. Mice infected with Theiler’s murine encephalomyelitis virus (TMEV) exhibit a chronic progressive clinical disease with similarities to MS.20 During the initial asymptomatic phase of disease, the initial immune response is to the TMEV capsid. However, 50 days post-infection, self-myelin proteoplipid protein epitope 139-151 (PLP139-151)-specific CD4+Th1 responses arise, concurrent with clinical symptoms.21,22 In late stage disease, T cell responses to other PLP epitopes (intra-molecular spread) and other myelin antigens such as MBP (inter-molecular spread), arise.22 Therefore, the initial response to the infectious pathogen can “spread” from pathogen-specific epitopes to self-epitopes following chronic tissue damage, and can lead to organ-specific autoimmune disease.
Immunofluorescence
Published in Guy Cox, Fundamentals of Fluorescence Imaging, 2019
The preabsorption control determines only the specificity of the antibody for the incubating protein or peptide and does not prove the specificity of the antibody for the protein in the tissue. An antibody can bind to any epitope that has the correct conformation, and this potentially includes the protein used for immunization, as well as any protein with a similar epitope. Therefore, the absorption control does not indicate that the protein to which the antibody binds in tissues is exactly the same protein that was used to generate the antibody [23]. The preadsorption control is meaningless for a monoclonal antibody since the immunogen will always bind it and always pass a preadsorption test, and for antibodies that have already been affinity purified (for the same reason) [2].
Production of codon-optimized Human papillomavirus type 52 L1 virus-like particles in Pichia pastoris BG10 expression system
Published in Preparative Biochemistry & Biotechnology, 2023
Kartika Sari Dewi, Sheila Chairunnisa, Sri Swasthikawati, Dian Fitria Agustiyanti, Apon Zainal Mustopa, Wien Kusharyoto, Ratih Asmana Ningrum
Interaction between antigen and antibody is essential in the humoral immune response against pathogenic invasion. Antigenic determinant or B-cell epitope is the part of an antigen that is recognized by secreted antibodies or B-cell receptors. Thus, identifying B-cell epitopes is crucial in developing vaccines, diagnostic tests, and therapeutics.[34] This study has selected one linear B-cell epitope based on several criteria, including antigenicity, surface accessibility, flexibility, and hydrophilicity. We assumed that the predicted epitope 476GLQARPKLKRPASSAPRTSTKKKKV500 is potential of inducing neutralizing antibody response against HPV52 pathogen. Moreover, the 3 D structure analysis of L1 protein using I-TASSER and PyMOL showed that the antigenic determinant or B-cell epitope was located in an exposed area which theoretically will be directly recognized by antibodies.
Natural latex serum: characterization and biocompatibility assessment using Galleria mellonella as an alternative in vivo model
Published in Journal of Biomaterials Science, Polymer Edition, 2022
Giovana Sant’Ana Pegorin Brasil, Patrícia Pimentel de Barros, Matheus Carlos Romeiro Miranda, Natan Roberto de Barros, Juliana Campos Junqueira, Alejandro Gomez, Rondinelli Donizetti Herculano, Ricardo José de Mendonça
Antigen recognition by antibody involves non-covalent reversible bonds of the variable fraction of the antibody with specific parts of the antigenic macromolecule, called epitopes [81]. Thus, this result confirms the presence of a protein domain that serves as an epitope for the interaction with this antibody, specific anti-FGFb, and can help explain the mechanism of action of the material on cell multiplication and angiogenesis.