Absence of immunologic memory in recipients of enhanced renal allografts.
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Specificity and memory are the defining characteristics of adaptive immune responses. Vaccines are predicated on the existence of immune memory, and the robustness of immune memory is a primary determinant of vaccine efficacy. How is immune memory maintained? Much progress has been made in this area over the past several years, and new human studies have added key insights into the longevity of B and T cell immune memory in the absence of antigen.
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Mathematical modelling is used to examine the effects of T cell apoptosis and memory differentiation dynamics on memory retention (memory stability). Apoptosis by cytokine deprivation induced death, and competition for survival signals are incorporated. Our models indicate that such population dependent processes are essential for the preservation of specific memory to previously encountered pathogens. Memory stability and vaccination properties improve significantly when population dependent mechanisms are present. These mechanisms work synergistically together to further improve memory characteristics. Our models emphasize the role of competitive cellular mechanisms in regulating repertoire structure and characteristics.
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T cell activation is a sustained process driven by antigen and cytokines, which results in the generation of large numbers of effector and memory cells. Recent experiments from different fields have shed light on the mechanisms that maintain the signaling process at the level of a single synapse between a T cell and an antigen-presenting cell, as well as at the level of a secondary lymphoid organ, in the course of the immune response. These findings explain the unique capacity of the immune system to discriminate between antigens from infectious and noninfectious agents.
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