The natural aging behavior of pure ternary Al‐Mg‐Si alloys is investigated by measuring hardness, electrical resistivity and positron lifetime, as well as carrying out thermal analysis and atom probe microscopy. It is found that several distinct temporal stages of natural aging can be distinguished in which one of these quantities shows a characteristic behavior and that these times coincide for many of these measurements. The rate of change in the measured data is correlated with proposed solute dynamics during natural aging for both aging that takes place prior to artificial aging (natural pre‐aging) and after artificial underaging (natural secondary aging) heat treatments. Controlling factors for solute dynamics are discussed.

The process of natural ageing in pure ternary Al-Mg-Si alloys was studied by positron annihilation lifetime spectroscopy in real time in order to clarify the sequence and kinetics of clustering and precipitation. It was found that natural ageing take place in at least 5 stages in these alloys, four of which were directly observed. This is interpreted as the result of complex Within the first 10 minutes after quenching, a period of nearly constant positron lifetime was found for those Mg-rich alloys that later show an insufficient hardness response to artificial ageing, the so-called 'negative effect'. The various processes observed could be described by two effective activation energies that were found by varying the ageing temperature from 10°C to 37°C.

Antigen presentation within the lymph node draining a site of infection is crucial for initiation of cytotoxic T cell responses. Precisely how this antigen presentation regulates T cell expansion in vivo is unclear. Here, we show that, in primary infection, antigen presentation peaks Ϸ3 days postinfection and then slowly decays until day 12. This prolonged antigen presentation is required for optimal expansion of naive CD8 ؉ T cells, because early ablation of dendritic cells reduces the later CD8 ؉ T cell response. Antigen presentation during secondary infection was 10-fold lower in magnitude and largely terminated by day 4 postinfection. Expansion of memory, but not naive, antigen-specific T cells was tightly controlled by perforin-dependent cytolysis of antigen-presenting cells. The ability of the memory T cells to remove antigenpresenting cells provides a negative-feedback loop to directly limit the duration of antigen presentation in vivo.dendritic cell ͉ immunological memory ͉ influenza virus ͉ T lymphocyte ͉ immunity P rotective immunity against pathogens depends on amplification of rare naive antigen-specific T cells that survive for long periods after initial exposure to the antigen. Antigenspecific naive T cells undergo more than a 1,000-fold expansion during the primary response, but 90-95% of the effector cells are rapidly eliminated by apoptosis, leaving a small number of surviving cells that form the stable memory pool (1-3). These few remaining memory cells are then poised to rapidly respond to a second encounter with the antigen, allowing massive reamplification of individual T cell populations. Despite this, memory T cell expansion also has a size constraint, and the immune system is obliged to sacrifice preexisting memory T cells to accommodate new ones.Part of the solution to regulation of the size of T cell populations lies in the rapid expansion and contraction of antigen-specific populations during a response. This is driven by the magnitude and duration of antigen presentation, but how antigen-presenting cell (APC) populations are themselves regulated in vivo to ensure optimal modulation of the size of T cell populations after primary and secondary infection is less clear (4, 5). One major paradigm, based largely on the coincident emergence of effector cytotoxic CD8 ϩ T cells (CTLs) with the quantitative reduction in antigen presentation, suggests that a regulatory feedback network exists whereby APCs are eliminated by responding T cells, thereby limiting the duration of stimulation (5-7). Restricting T cell activation and amplification would be an essential checkpoint in preventing chronic lymphocyte activation and associated immunopathology (8). However, this mechanism may not universally apply in all immune responses. Ablation of antigen presentation at various time points during primary Listeria monocytogenes and herpes simplex-1 infection has highlighted that more prolonged antigen presentation can positively influence the size of the T cell expansion (4, 9, 10). Interestingly, APCs th...