The increase is accompanied by affinity maturation which induces the survival of B cells that bind to the particular antigen with high affinity. However, with each cycle, the number of surviving memory cells increases. A small minority survives as memory cells that can recognize only the same epitope. Most of such B cells differentiate into plasma cells that secrete antibodies into blood that bind the same epitope that elicited proliferation in the first place. Upon encountering its specific antigen, a single B cell, or a clone of cells with shared specificity, divides to produce many B cells. The great diversity in immune response comes about due to the up to 109 clones with specificities for recognizing different antigens. Such clonality has important consequences, as immunogenic memory relies on it. All B cells derive from a particular cell, and as such, the antibodies and their differentiated progenies can recognize and/or bind the same specific surface components composed of biological macromolecules ( epitope ) of a given antigen. In 1958, Sir Gustav Nossal and Joshua Lederberg showed that one B cell always produces only one antibody, which was the first evidence for clonal selection theory.ī cells exist as clones. One clone acts immediately to combat infection whilst the other is longer lasting, remaining in the immune system for a long time, which results in immunity to that antigen. ” Burnet explained immunological memory as the cloning of two types of lymphocyte. Talmage, worked on this model and was the first to name it “clonal selection theory. Australian immunologist Frank Macfarlane Burnet, with input from David W. This selection of only one type of lymphocyte results in it being cloned or reproduced by the body extensively to ensure there are enough antibodies produced to inhibit and prevent infection. The entrance of an antigen into the body results in the selection of only one type of lymphocyte to match it and produce a corresponding antibody to destroy the antigen. In 1954, Danish immunologist Niels Jerne put forward a hypothesis which stated that there is already a vast array of lymphocytes in the body prior to any infection. Those lymphocytes bearing receptors for self molecules will be deleted at an early stage.The differentiated effector cells derived from an activated lymphocyte will bear receptors of identical specificity as the parental cell.Receptor occupation is required for cell activation.Each lymphocyte bears a single type of receptor with a unique specificity (by V(D)J recombination).Most of these will never encounter a matching 5) foreign antigen, but those that do are activated and produce 6) many clones of themselves.įour predictions of the clonal selection hypothesis Those that bind to 3) antigens from the body’s own tissues are destroyed, while the rest mature into 4) inactive lymphocytes. Figure: A schematic view of clonal selection: Clonal selection of lymphocytes: 1) A hematopoietic stem cell undergoes differentiation and genetic rearrangement to produce 2) immature lymphocytes with many different antigen receptors. The clonal selection hypothesis has become a widely accepted model for how the immune system responds to infection and how certain types of B and T lymphocytes are selected for destruction of specific antigens invading the body. clone: A group of identical cells derived from a single cell.Binding of Ag to a cell activates the cell, causing a proliferation of clone daughter cells. clonal selection: An hypothesis which states that an individual lymphocyte (specifically, a B cell) expresses receptors specific to the distinct antigen, determined before the antibody ever encounters the antigen.The advanced methodology, termed B-cell targeting, multitargeting and stereospecific targeting, may be applicable to simultaneous production of monoclonal antibodies, selective production of stereospecific monoclonal antibodies, and also to efficient generation of human monoclonal antibodies for clinical purposes.\) To overcome this problem, we have developed a new hybridoma technology that involves preselection of B lymphocytes with target antigens based on immunoglobulin receptors and selective fusion of B cell-myeloma cell complexes with electrical pulses. However, the methods generally do not necessarily result in selective fusion of target B lymphocytes with myeloma cells. For standard generation of hybridoma cells, B lymphocytes must be somatically fused with myeloma cells using various technologies. Hybridoma technology features effective usage of innate functions of both immune cells and cancers, allowing production of hybridoma cells, which continuously generate monoclonal antibodies specific to antigens of interest.
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