Evaluate clonal selection hypothesis in terms of autoimmunity and immunological memory
Clonal selection is the theory that lymphocytes have antigen receptors before they are activated, and that spontaneous mutations during clonal expansion lead to lymphocytes with high antigen-binding affinities. It is a theory that a single lymphocyte (specifically, a B cell) expresses antigen-specific receptors that are determined before the antibody ever meets the antigen. As Ag binds to a chromosome, it stimulates it, allowing clone daughter cells to proliferate.
Negative selection in the bone marrow produces central tolerance in B cells. Before leaving the bone marrow, immature B cells are screened for auto-reactivity. Immature B cells with BCRs that bind to self-antigens too strongly will not be destroyed. Random mutations during clonal expansion induce the development of B cells with an improved antibody-binding affinity for their antigens during clonal selection. The clonal selection hypothesis could understand why secondary immune responses are so effective in avoiding reinfection by the same pathogen.
The capacity of B and T cells to generate long-lived memory cells that protect against particular pathogens is referred to as immunological memory. Any of the offspring of B and T cells will become long-lived memory cells until they begin to reproduce. Memory cells keep track of any specific pathogens encountered during an animal's lifespan and may mount a robust defense if the pathogen resurfaces. IgG antibodies provided by the mother during fetal development and by breast milk provide passive immunity. This recollection is only temporary, but it supports the newborn before it develops its own adaptive immune system. Owing to frequent strain variations and the difficulty of developing an immunization that is effective enough to function but not strong enough to induce infection, vaccines do not exist for any pathogen.