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An epitope, also known as antigenic determinant, is the part of an antigen that is recognized by the immune system, specifically by antibodies, B cells, or T cells. The part of an antibody that binds to the epitope is called a paratope .
Conversely, epitope spreading could be due to target antigens being physically linked intracellularly as members of a complex to self antigen. The result of this is an autoimmune response that is triggered by exogenous antigen that progresses to a truly autoimmune response against mimicked self antigen and other antigens. [ 18 ]
In immunology, epitope mapping is the process of experimentally identifying the binding site, or epitope, of an antibody on its target antigen (usually, on a protein). [ 1 ] [ 2 ] [ 3 ] Identification and characterization of antibody binding sites aid in the discovery and development of new therapeutics , vaccines , and diagnostics .
Likewise, T Cell epitopes can cause unwanted immunogenicity, including the development of ADAs. A key determinant in T cell epitope immunogenicity is the binding strength of T cell epitopes to major histocompatibility complexes (MHC or HLA) molecules. Epitopes with higher binding affinities are more likely to be displayed on the surface of a cell.
In a cell, protein molecules of the host's own phenotype or of other biologic entities are continually synthesized and degraded. Each MHC molecule on the cell surface displays a small peptide (a molecular fraction of a protein) called an epitope. [3] The presented self-antigens prevent an organism's immune system from targeting its own cells ...
Recognition of epitopes in a linear fashion. Note: the same (colored) segment of protein can be a part of more than one epitopes. In immunology, a linear epitope (also sequential epitope) is an epitope—a binding site on an antigen—that is recognized by antibodies by its linear sequence of amino acids (i.e. primary structure).
Immune complexes may themselves cause illness when they are deposited in organs, for example, in certain forms of vasculitis. This is the third form of hypersensitivity in the Gell-Coombs classification, called type III hypersensitivity . [ 4 ]
As IgM antibodies are expressed early in a B cell response, they are rarely highly mutated and have broad antigen reactivity thus providing an early response to a wide range of antigens without the need for T cell help. [5] IgD isotypes are expressed on naive B cells as they leave bone marrow and populate secondary lymphoid organs.