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Report from the second cytomegalovirus and immunosenescence workshop.
Full text linkThe Second International Workshop on CMV & Immunosenescence was held in Cambridge, UK, 2-4th December, 2010. The presentations covered four separate sessions: cytomegalovirus and T cell phenotypes; T cell memory frequency, inflation and immunosenescence; cytomegalovirus in aging, mortality and disease states; and the immunobiology of cytomegalovirus-specific T cells and effects of the virus on vaccination. This commentary summarizes the major findings of these presentations and references subsequently published work from the presenter laboratory where appropriate and draws together major themes that were subsequently discussed along with new areas of interest that were highlighted by this discussion
Age-related increases in DNA damage and mutations in T cells in vivo and in vitro: contributors to alterations in T cell-mediated immune responses?
No full textMicrosatellite instability and compromised mismatch repair gene expression during in vitro passaging of monoclonal human T lymphocytes.
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Altered expression of mismatch repair proteins associated with acquisition of microsatellite instability in a clonal model of human T lymphocyte aging.
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Role of TLR Polymorphisms in Aging and Age-Related Diseases
No full textInnate immunity provides the first line of host defense against infection by
recognizing and killing microbes, and simultaneously activating an instructive
immune response. Toll-like receptors (TLRs) are principal mediators of rapid
microbial recognition, and they mainly function by detecting exogenous
pathogen-associated molecular patterns. Recognition of their ligands actives
signaling ways, which culminate in evocating acute host responses, involved in
killing pathogens. Here, we describe the involvement of TLR4 polymorphisms in
aging, and particularly in immunosenescence and age-related diseases,
suggesting the crucial role of molecules of innate immunity in the pathophysiology
of these diseases. Accordingly, we observed that proinflammatory alleles
may be related to unsuccessful aging, such as Alzheimer’s disease, prostate
cancer, diabetes, cardiovascular diseases (i.e., atherosclerosis, aneurysm), and
the anti-inflammatory alleles may reciprocally result in increased longevity and
successful aging. Finally, a possible therapeutic approach to delay age-related
diseases is outlined
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