Abstract
Human immune senescence accompanies with the physical and physiological frailty. The functional change and shift of NK, NKT and T cell subsets by aging have been widely studied. However, it remains largely unclear how the aging and disease conditions affect the distribution of lymphocytes. In the present study, 233 subjects with age range from 20 to 87 year old, including healthy people, people with chronic gastrointestinal tract disease or cancers were investigated. We found that the proportion of NK cells, CD8+ T cells and NKT cells remained relatively unchanged with aging. However, NKG2D and CD16 expression level on NK cells decreased with aging indicating impaired NK cell function. Surprisingly, the proportion of NK, NKT and T cells all declined with deteriorating health status from health to chronic gastrointestinal tract disease and cancer. Furthermore, cytokine and chemokine profiles changed with aging, but did not vary with different health status. Our results highlight new evidence for a continuum of change during immunologic aging and show unique data for variations of NK cells, CD8+ T cells, NKT cells, and cytokine microenvironment with human aging and health status transformation.
Highlights
Immunosenescence is described as a decline in the normal function of the immune system associated with physiologic aging, which leads to increased susceptibility to infection, cancer and autoimmune diseases in aged organisms, including humans [1]
We found that the proportion of Natural Killer (NK) cells, CD8+ T cells and Natural killer T (NKT) cells remained relatively unchanged with aging
We investigated the changes of lymphocyte subsets and cytokines with aging without eliminating the health status, which includes healthy individuals and individuals with chronic gastrointestinal tract diseases or gastrointestinal tract cancer
Summary
Immunosenescence is described as a decline in the normal function of the immune system associated with physiologic aging, which leads to increased susceptibility to infection, cancer and autoimmune diseases in aged organisms, including humans [1]. Dysfunction has been defined for both innate immune system providing natural resistance to infections and tumorigenesis, and the adaptive system for acquired and long-preserving immunity. The aging of adaptive immunity has been widely appreciated, because the atrophy of thymus starts with birth and accelerates during adolescence [2]. This modification accompanies with a decrease in the absolute number of T lymphocytes (CD3+ T cells), including CD4+ T and especially CD8+ T subsets [3]. CD28+ T cells lose the CD28 receptor due to repeated antigenic stimulations and become replicative senescence with a characters of shortened telomeres and reduced proliferative capacity [5]
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