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Immune Reconstitution after Hematopoietic Stem Cell Transplantation
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Andreas Thiel, Tobias Alexander, Christian A. Schmidt, Falk Hiepe, Renate Arnold, Andreas Radbruch, Larissa Verda, Richard K. Burt
NK cells are elevated at birth and then normalize within weeks postpartum. Absolute numbers of NK cells remain stable until old age when their number increases (Fig. 5). In the first year of life, total T and B cell number as well as CD4+ CD45RA+ naïve T cells increase to provide a large pool of cells ready to recognize and respond to antigens.12,79-81 The first year of life is, therefore, marked by rapid development of a thymic-derived immune system. With onset of puberty, the size and architecture of the thymus involutes and thymic lymphopoiesis declines. Age-related reduction of thymic T cell development appears to be the key event associated with subsequent age-related change that has been correctly or incorrectly termed “immunosenescence”.82-85
AI and Autoimmunity
Published in Louis J. Catania, AI for Immunology, 2021
AI technologies are starting to deliver promising results in different fields of aging and longevity research. The most important alterations of aging occur in the adaptive immune system and involve T-cells. Many of these alterations are assumed to decrease capacity of the immune system to combat an emerging or progressing tumor. The declining function of the immune system is known as immunosenescence and leads to a higher incidence of infection, cancer, and autoimmune disease-related mortalities in the elderly population.12
Effects of Whole Body Vibration on the Elderly
Published in Redha Taiar, Christiano Bittencourt Machado, Xavier Chiementin, Mario Bernardo-Filho, Whole Body Vibrations, 2019
Maíra Florentino Pessoa, Helga C. Muniz de Souza, Helen K. Bastos Fuzari, Patrícia E. M. Marinho, Armèle Dornelas de Andrade
The immune system of the elderly undergoes transformations and their immune response patterns are age dependent. Changes that occur from the age of 50 have received special attention due to their clinical impact, and such changes have been globally known as immune senescence or immunosenescence.
Ex vivo treatment with fucoidan of mononuclear cells from SARS-CoV-2 infected patients
Published in International Journal of Environmental Health Research, 2022
K. J. G. Díaz-Resendiz, G. A. Toledo-Ibarra, R. Ruiz-Manzano, D.A. Giron Perez, C.E. Covantes-Rosales, A. B. Benitez-Trinidad, K. M Ramirez-Ibarra, A. T. Hermosillo Escobedo, I. González-Navarro, G.H. Ventura-Ramón, A. Romero Castro, D. Alam Escamilla, A. Y. Bueno-Duran, Manuel Iván Girón-Pérez
Besides, cellular senescence was also evaluated (Figure 3), which plays a beneficial role by preventing tumor development through cell proliferation suppression mechanisms and is associated with tissue regeneration, particularly in epithelial cells and fibroblasts (Lee et al. 2015). Concerning fucoidan, this compound decreased the senescence of mononuclear cells from endothelial colony-forming cells isolated from human umbilical cord blood, indicating that fucoidan rescues these cells from replicative senescence (Lee et al. 2015). As for the immune system, senescence is an aging process often called immunosenescence, that increases cancer, infection, and autoimmune disease susceptibility, especially in older individuals (Prelog 2006; Falci et al. 2013; Pietrobon et al. 2020). In SARS-CoV-2 infected patients, the immunosenescence process appears to play a significant role in COVID-19 prognosis, associated with the increased inflammatory cytokines production during this disease (Pietrobon et al. 2020), thus we evaluate the senescence in immune cells (PBMCs). Obtained results showed that neither the infection nor the treatment with fucoidan exerted an effect on cell senescence on PBMCs from any of the studied groups. However, further tests must be performed to evaluate the association between immunosenescence and the severity of COVID-19 in immune cells, as well as its association with patient age.
From Infections to Anthropogenic Inflicted Pathologies: Involvement of Immune Balance
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Florence Lee, David A Lawrence
A key feature of immunosenescence is a persistent low-grade inflammation, and there is evidence indicating that this is due to a reduction in naïve T cells and an accumulation of CD8 cytotoxic T cells that produce pro-inflammatory cytokines including IFNγ (Nikolich-Žugich et al. 2012). There is some evidence pointing to the β-herpesvirus CMV as a mitigating factor in the cause of the persistent low-grade inflammation seen in older populations (Vescovini et al. 2007). CMV is a common pathogen that affects more than half of the United States adult population (CDC 2010). Similar to shingles virus, after recovery of the primary infection, CMV is inhibited in immunocompetent hosts, where a steady stream of immune supervision manages it. However, investigators found a significant amount of CMV-specific T cell proliferation that overburdens an older individual’s immune repertoire, demonstrating that more than 5% of T cells are trying to keep CMV at bay (Khan et al. 2002; Sylwester et al. 2005). Immune decline with age is partially due to an imbalance between naïve and memory T cells. Memory T cells with specificity toward endogenous viruses, such as CMV, create an excess of memory T cells and inflammation, which initiates a contraction of the T cell repertoire and lessens immunity to new antigens (Weltevrede et al. 2016; Wertheimer et al. 2014). When battling chronic infections producing inflammation, the host’s resources, instead of being used for somatic maintenance are utilized for immune control of infection and inflammation.