Immune function and dysfunction in relation to aging

Cheney, Kay E.; Walford, Roy L.

doi:10.1016/0024-3205(74)90090-3

Cited by 11 publications

(3 citation statements)

References 20 publications

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“…• Inflammation is believed to be a major factor in aging of the nervous system due to dysfunction of the immune system, inflammatory processes and toxic activity of immune modulators (Cheney and Walford, 1974). • In a clearly defined senescence program, activity of defined gene products is a cause of progression of aging leading to a limited replicative life span of somatic cells (replicative senescence; Hayflick and Moorhead, 1961).…”

Section: Aging Of the Brain And Molecular Theories Of Agingmentioning

confidence: 99%

Brain aging and late-onset Alzheimer's disease: many open questions

Behl

2012

Int. Psychogeriatr.

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Despite decades of research in the field of Alzheimer's disease (AD), a real understanding of its molecular pathophysiology and treatments relevant to the day-to-day lives of patients remain out of reach. Research has, with good reason, focused on certain key pathways and potential mechanisms, but sometimes this has been at the expense of work on other theories, which may be slowing down progress in this field. Interesting theories at present include oxidative stress and caloric restriction. Work on the Aβ cascade should continue but with a shift in focus to its intracellular effects and an awareness that additional pathogenetic factors and processes must be involved--most importantly, brain aging. Hyperphosphorylation of tau, for instance, provides another interesting pathway, with one old drug showing promise in this regard. Moreover, work in epigenetics and on protein homeostasis has produced interesting findings and both lines of investigation may reveal suitable targets for future intervention. Taken together, analysis of the biochemistry of aged neurons and the interplay with pathways of neurodegeneration may lead to a better understanding of AD and how to treat and prevent this condition.

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Section: Aging Of the Brain And Molecular Theories Of Agingmentioning

confidence: 99%

Brain aging and late-onset Alzheimer's disease: many open questions

Behl

2012

Int. Psychogeriatr.

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“…

One manifestation of the aging process is a gradual decrease in the ability of aged individuals to mount a humoral immune response (1)(2)(3)(4) . Studies at the cellular level demonstrated that much of this diminished reactivity can be attributed to the environment of the aged animal itself, which limits the responsiveness of the available B cells (3)(4)(5)(6)(7)(8) .This laboratory (9) and others (10) have observed that, after immunization with a given antigen, immunoregulatory mechanisms develop that are best evidenced by the suppression of the capacity of primary B cells to respond to the same antigenic determinant . In our experiments, this suppression appears to be specific for idiotypic determinants expressed on the primary B cell receptors, because such suppression obtains only for B cells specific for the immunizing antigen and is not capable of suppressing B cells of murine strains differing in the idiotype-allotype genetic locus (9) .

…”

mentioning

confidence: 99%

“…One manifestation of the aging process is a gradual decrease in the ability of aged individuals to mount a humoral immune response (1)(2)(3)(4) . Studies at the cellular level demonstrated that much of this diminished reactivity can be attributed to the environment of the aged animal itself, which limits the responsiveness of the available B cells (3)(4)(5)(6)(7)(8) .…”

mentioning

confidence: 99%

Antibody-specific immunoregulation and the immunodeficiency of aging.

Klinman¹

1981

The Journal of Experimental Medicine

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One manifestation of the aging process is a gradual decrease in the ability of aged individuals to mount a humoral immune response (1-4) . Studies at the cellular level demonstrated that much of this diminished reactivity can be attributed to the environment of the aged animal itself, which limits the responsiveness of the available B cells (3)(4)(5)(6)(7)(8) .This laboratory (9) and others (10) have observed that, after immunization with a given antigen, immunoregulatory mechanisms develop that are best evidenced by the suppression of the capacity of primary B cells to respond to the same antigenic determinant . In our experiments, this suppression appears to be specific for idiotypic determinants expressed on the primary B cell receptors, because such suppression obtains only for B cells specific for the immunizing antigen and is not capable of suppressing B cells of murine strains differing in the idiotype-allotype genetic locus (9) . Thus, for example, BALB/c mice immunized with 2,4-dinitrophenyl (DNP)-hemocyanin and subsequently used as the adoptive irradiated hosts in B cell transfer experiments suppress the response of primary BALB/c DNP-specific B cells but facilitate the response of primary B cells from B10 .D2 or CB20 donors that differ from BALB/c mice in the immunoglobulin heavy chain locus .Because the effects of this antibody-specific immunoregulation appear to be longlasting, we reasoned that the antigenic experiences of a lifetime could eventuate in the accumulation of suppressive recognition for a large proportion of an individual's normal primary B cell repertoire . The experiments described in this report test this hypothesis . We have assessed the capacity of the environment or cells of aged individuals, who have never been immunized to the hapten DNP, to suppress the responses of primary DNP-specific B cells derived from young syngeneic or allotype allogeneic donors. The results indicate that aged individuals have indeed accumulated the capacity to suppress the responses of syngeneic primary B cells but not the responses of primary B cells differing in the heavy chain allotype locus . Materials and MethodsAntigens. The proteins hemocyanin (Hy) and bovine serum albumin, and the antigens DNPt o-Hy and DNPIS-bovine serum albumin were prepared and characterized as previously described (9) .Animals and Immunization . 24-26-mo-old BALB/c male mice and their 2-mo-old cohorts were obtained from the Charles River Breeding Laboratories, Inc ., Wilmington, Mass. 2-mo-old * Supported by grants AGO 1514 and AGO 1743 from the United States Public Health Service . J . Exp. MED.

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Animal Models for Evaluating Xenobiotic Growth Hormone Secretagogue Activity

Walker¹,

Bercu²

1996

Growth Hormone Secretagogues

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Immune function and dysfunction in relation to aging

Cited by 11 publications

References 20 publications

Brain aging and late-onset Alzheimer's disease: many open questions

Brain aging and late-onset Alzheimer's disease: many open questions

Antibody-specific immunoregulation and the immunodeficiency of aging.

Animal Models for Evaluating Xenobiotic Growth Hormone Secretagogue Activity

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