University College Cork was the setting or the recent 670th meeting of the Biochemical Society this year, a meeting at which the Biochemical Immunology Group Colloquium hosted a one-day session on Ageing and the Immune system. The session was chaired in the morning by Dr David Kipling (Cardiff) and in the afternoon by Dr Janet Lord (Birmingham) and was successful in providing both an overview of current work and a snapshot of recent advances.
The session started with a presentation by Dr Richard Faragher (Brighton). Dr Faragher presented data on the cell turnover rates in different tissues and spoke of the linkage between cells senescence and human ageing. He cited evidence suggesting that senescence was an anti-cancer mechanism and made a strong case for the role of the telomere shortening in the induction of senescence in human tissue.
The role of senescence as a barrier to cancer was taken up by the next speaker, Dr E.K. Parkinson (CRC Beatson labs Glasgow) who was addressing questions as to the mechanisms of senescence in normal human keratinocytes and how this is overcome to produce immortal variants. He presented data from human cell lines which showed that immortal keratinocytes usually showed cor rupted p53 and p16 function and have high levels of telomerase.
This was followed by Dr Simon Cook (Babraham Institute Cambridge) who has been studying the role of different Ras-dependent signalling pathways in regulating cell cycle re-entry and proliferation. Dr Cook presented work on analysing the stress-activated protein kinases in cell cycle arrest, senescence and apoptosis using a series of *MEKK-ER* fusions.
The next speaker, Professor R. Miller (Michigan USA) gave an overview of changes in the immune system with age. He put forward the view that because mice have very long telomeres the decline in the immune function in the mouse could not be adequately explained by telomere shortening alone. He then went on to present data on defects in the ability of the theta isoenzyme of PK-C to move to the region of the T cell/Antigen Presenting Cell interface. Finally he discussed differences in a number of immunological parameters of mice derived from ecological niches of low hazard compared with a normal laboratory adapted strain.
This was then followed by an excellent presentation of work by Dr U.M. Martens (Freiburg) on telomere measurements in haemopoeitic cells. Dr Martens revealed an elegant study on the telomere length in single cells in which measurement was carried out using quantitative fluorescent in situ hybridisation (Q-FISH) and an extension of this method to enable flow cytometric analysis (Flow FISH).
The next presentation from Dr R. Aspinall (Imperial, London) who explained that the thymus atrophied with age and as a consequence its output declined but despite this the number of T cells in the peripheral T cell pool was maintained. This could be achieved by the proliferation of T cells in the peripheral T cell pool but would eventually lead to many of these cells reaching their replicative limit and hence to immune senescence. This problem may be overcome by reversing thymic atrophy, increasing thymic output providing new T cells to refresh the peripheral T cell pool. He then presented data on the causes of thymic atrophy and the use of IL-7 to induce thymopoiesis in ageing mice.
The final speaker in the session was Dr Arne Akbar who discussed homeostatic mechanisms to maintain T cell numbers within defined limits especially after infections with Epstein Barr virus. After infection the massive increase in CD8 cells is reduced by apoptosis but some persist as memory cells. The telomeres in these cells are not as reduced as expected indicating that there may be some telomerase activity which enables these cells to persist for prolonged periods as memory cells.