Role of the Immune System in Aging

Makinodan, Takashi

doi:10.1007/978-1-4684-3734-8_19

Cited by 15 publications

(9 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been proposed that the altered responses of T cells from aged animals result from the accumulation of memory T cells. The percentages of memory T cells increase with aging, which is supported by the markedly increased expression of CD44, as well as the decreased expression of CD45RB and CD62L on T cells in aged mice [40,41]. In accordance with previous reports, normal percentages and total cell numbers of CD4 or CD8 cells in spleens and lymph nodes and significantly lower percentages of CD4 ϩ T cells in the peripheral blood were observed in 20-month-old mice.…”

Section: Discussionsupporting

confidence: 93%

Changes of CD4+CD25+Foxp3+ regulatory T cells in aged Balb/c mice

Zhao

Sun

Wang

et al. 2007

Journal of Leukocyte Biology

139

113

View full text Add to dashboard Cite

A progressive decline in the integrity of the immune system is one of the physiologic changes during aging. The frequency of autoimmune diseases or immune disorders increases in the aging population, but the state of regulatory T (Treg) cells in aged individuals has not been well determined. In the present study, we investigated the levels, phenotypes, and function of CD4(+)CD25(+) Treg cells in Balb/c mice, which were older than 20 months. Significantly enhanced percentages of CD4(+)CD25(+) Treg cells in the periphery (blood, spleen, and lymph nodes) of the aged mice were observed. These Treg cells showed modified Vbeta family distribution, reduced levels of CD45 receptor B and CD62 ligand molecules, as well as normal levels of forkhead box p3. However, when the inhibiting function of Treg cells was assayed in the in vitro assays and in a delayed-type hypersensitivity (DTH) model, CD4(+)CD25(+) Treg cells of aged mice displayed significantly lower inhibiting ability on alloantigen-induced DTH reaction or cytokine productions (IL-2 and IFN-gamma) but not cell proliferation of effector T cells, as compared with CD4(+)CD25(+) Treg cells of young mice. In addition, the percentages of CD4(+)CD8(-)CD25(+) Treg cells in the thymi of aged mice increased significantly, but their total cell numbers decreased markedly in these mice. Our present studies indicated collectively that the percentages, phenotypes, the size of TCR repertoire, and function of CD4(+)CD25(+) Treg cells were altered significantly with aging in mice. The functional defects of CD4(+)CD25(+) Treg cells may shed light on the role of CD4(+)CD25(+) Treg cells in the increased sensitivity to autoimmune diseases of aged populations.

show abstract

Section: Discussionsupporting

confidence: 93%

Changes of CD4+CD25+Foxp3+ regulatory T cells in aged Balb/c mice

Zhao

Sun

Wang

et al. 2007

Journal of Leukocyte Biology

139

113

View full text Add to dashboard Cite

show abstract

“…This transitional shift in WBC pattern is also observed to be similar in humans. [4][5][6][7][8] The fact that under present experimental conditions, we observed similar percentages of immune cell subpopulations as previously reported in adult rats and the pattern of alteration in aged rats suggests that flow cytometry method was used appropriately.…”

Section: Discussionsupporting

confidence: 89%

“…Many studies had demonstrated attenuated immunity in old age subjects correlated to the decline of T cell proliferation and B cell antibody production during aging, with increasing risks to infections observed in elderly people. [4][5][6][7][8][9][10] The age-dependent pattern changes in WBC distribution can be observed in both humans and rodents, although the percentage changes in each species differ slightly. Studies conducted by Feldman 25) and Mohr 26) on rats Distribution of WBC in ovary-intact rats before and after MBFP (3 g/kg/d for 6 weeks) (A), E 2 (50 mg/kg/d for 6 weeks) (B) and water (10 ml/kg/d for 6 weeks) (C).…”

Section: Discussionmentioning

confidence: 99%

“…The decline is due to changes in hormone levels 3) and in the immune cells, where cell loss, shift in the proportion of subpopulations, and qualitative cellular changes have all been detected. [4][5][6] Age related immune decline has also been observed in the gastrointestinal-associated mucosa of humans. Older subjects exhibited lower levels of IL-2 secretion and IgA antibody production in response to stimuli, and showed slower cell proliferation and differentiation in peripheral blood mononuclear cells and lamina propria lymphocytes than those of younger subjects.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Effects of Bak Foong Pills and Menoease Pills on White Blood Cell Distribution in Old Age Female Rats

Gou

Rowlands

et al. 2003

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

The immune system is a defence mechanism that protects the body from infectious pathogens, such as viruses, bacteria, fungi, protozoa and multicellular parasites found in the environment.1) Immune responses are mediated by a variety of cells that originates from the bone marrow and differentiates into specific cell types in primary lymphoid organs. Some cells can be differentiated into white blood cells (WBC), which can circulate into the bloodstream or migrate into specific tissues for homing. The major classes of WBC include: antibody producing B lymphocytes and cytokine-releasing and cytotoxic T lymphocytes, phagocytic monocytes and macrophages, heavily granulated neutrophils, eosinophils and basophils, and other auxillary mast cells, dendritic cells and platelets. Together, these cells form a main part of the immune system of our body against environmental assaults.2)The immune system declines with age, an onset that can occur as early as when an individual reaches sexual maturity. The decline is due to changes in hormone levels 3) and in the immune cells, where cell loss, shift in the proportion of subpopulations, and qualitative cellular changes have all been detected. [4][5][6] Age related immune decline has also been observed in the gastrointestinal-associated mucosa of humans. Older subjects exhibited lower levels of IL-2 secretion and IgA antibody production in response to stimuli, and showed slower cell proliferation and differentiation in peripheral blood mononuclear cells and lamina propria lymphocytes than those of younger subjects. 7,8) Moreover, individuals with less efficient immune systems have been observed to have greater chance to bacterial infections. 9,10) Although the links between sex hormones, such as estrogen (E 2 ), and immune status in aging has not been firmly established, there is evidence showing a correlation between reduced hormone levels in post-menopausal women associated with increased risk of pathological and malignant diseases, such as higher blood pressure and cholesterol, osteoporosis, cardiovascular diseases, endometrial cancers and Alzheimer's diseases. [9][10][11][12][13][14][15] Recent findings from women receiving hormone replacement therapy (HRT) suggest preservation or improvement of immune function associated with HRT by regulating the release of cytokines and cytokine secreting cells. 16,17) In premenopausal women, there were high numbers of cytokine-releasing cells, whereas in post-menopausal women, there was a reduction in number of cytokines-secreting cells. Women receiving HRT, on the other hand, produced higher lymphocyte proliferation than untreated controls and showed slower signs to the development of post-menopausal symptoms. 11,16,17) These findings suggest that HRT with E 2 prevents post-menopausal women from an aberration of immune system by regulating cytokine genes and growth hormones and improving the balance of T-lymphocytes immune reactions. 12,18,19) Bak Foong Pills (BFP, also known as Bai Feng Wan), is a traditional Chinese medicine composed of...

show abstract

“…Their rationales range from explaining aging by a committed progressive breakdown of functions of immunocompetent cells and their clonal exhaustion (WALFORD 1969;BURNET 1970;HOLLIDAY et al 1981) to explaining progressive loss of immunity by phenomena of aging such as: (a) somatic mutation (ORGEL 1963(ORGEL , 1973; (b) error in replication or repair of DNA (JOHNSON and STREHLER 1972;HART and SETLOW 1974); (c) error proneness of DNA polymerases and related enzymes (BURNET 1976); respiration-dependent injury to the mitochondrial genome (FLEMING et al 1982) in other cells than immunocompetent cells. Several excellent recent reviews have compiled mutual associations between age and immune system of different species, including man (WALFORD 1969;MAKINODAN et al 1971 ;KAY and MAKINO-DAN 1976;MAKINODAN and YUNIS 1977;YUNIS et al 1978;GOOD et al 1979;KISHIMOTO and MITSUYA 1980;WILLIAMS et al 1980;LEECH 1980;WEKSLER 1980;MAKINODAN 1980;KAY and MAKINODAN 1981). In particular, T cell system-dependent immune functions seem to decline with age (Table 1), whereas functions of macrophages and B cells do not appear to be impaired KAY and MAKINODAN 1981;BENNER et al 1981).…”

mentioning

confidence: 97%