Impaired Antigen Presenting Function of Macrophages from Aged Mice

Vĕtvická,; Tlaskalová‐Hogenová, Helena; Pospı́šil, M.

doi:10.3109/08820138509042005

Cited by 33 publications

(10 citation statements)

References 19 publications

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“…Age-related alterations in the functional capacity of macrophages are likely to contribute significantly to loss of natural immunity with dysregulated cytokine production and antigen-presenting ability (Vetvicka et al, 1985;Bradley et al, 1989). Specifically, a defective PKC system underlies the age-associated impairment of a number of these processes (Corsini et al, 1999).…”

Section: Discussionmentioning

confidence: 97%

The Sex Steroid Precursor DHEA Accelerates Cutaneous Wound Healing Via the Estrogen Receptors

Mills¹,

Ashworth²,

Gilliver³

et al. 2005

Journal of Investigative Dermatology

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Age-related impaired wound healing states lead to substantial morbidity and cost, with treatment in the USA resulting in an expenditure of over $9 billion per annum. Dehydroepiandrosterone (DHEA) is a ubiquitous adrenal hormone with immunomodulatory properties whose levels decline significantly with advanced age in humans. Conversion of DHEA locally to downstream steroid hormones leads to estrogenic and/or androgenic effects which may be important in age-related skin homeostasis, and which would avoid systemic adverse effects related to estrogen. We report that systemic DHEA levels are strongly associated with protection against chronic venous ulceration in humans. DHEA accelerated impaired healing in an impaired healing model (mice rendered hypogonadal) associated with increased matrix deposition and dampens the exaggerated inflammatory response. Such effects were mediated by local conversion of DHEA to estrogen, acting through the estrogen receptor, and vitro studies suggest a direct effect on specific pro-inflammatory cytokine production by macrophages via mitogen activated kinase (MAP) and phosphatidylinositol 3 (PI3) kinase pathways. In addition, we show that local injection of DHEA accelerates impaired healing in an ageing mouse colony. We suggest that exogenous application of DHEA accelerates impaired wound repair, results which may be applicable to the prophylaxis and treatment of human impaired wound healing states.

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Section: Discussionmentioning

confidence: 97%

The Sex Steroid Precursor DHEA Accelerates Cutaneous Wound Healing Via the Estrogen Receptors

Mills¹,

Ashworth²,

Gilliver³

et al. 2005

Journal of Investigative Dermatology

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“…Accessory function of peritoneal macrophages from aged mice has been found to be either decreased [39] or comparable [40] to that of young animals. In humans, Schwab et al [6] found that the age-associated defect in lymphocyte responses to the monoclonal antibody OKT3 was similar whether mono cytes from young or old donors were used demonstrating that there was no accessory defect of monocytes from the elderly for this stimulus.…”

Section: Discussionmentioning

confidence: 99%

Accessory Function and Properties of Monocytes from Healthy Elderly Humans for T Lymphocyte Responses to Mitogen and Antigen

Rich

Mincek²,

Armitage³

et al. 1993

Gerontology

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The waning of cell-mediated immunity during aging has been attributed primarily to defects in T lymphocyte properties and functions. We assessed the potential contribution of accessory dysfunction of monocytes from the elderly on responses of T cells to phytohemagglutinin (PHA) and to tetanus toxoid after in vivo boosting. Accessory function of monocytes from the elderly subjects for T lymphocyte responses to tetanus toxoid was comparable to the young. Expression of the cytokines interleukin-1 interleukin-6 and tumor necrosis factor, the cell adhesion molecules ICAM-1 and LFA-3 and the class II major histocompatibility molecule HLA-DR by monocytes from the elderly and young subjects was similar. T lymphocytes from the elderly responded poorly to PHA. Monocytes from the elderly had a decreased accessory function for PHA-stimulated T cells from young, third donors. Thus, although many accessory properties of monocytes from the elderly are normal, the monocyte and T lymphocyte defects in the elderly for mitogen may represent interactive factors in cell-mediated immunity during aging.

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“…It has been reported that antigenpulsed macrophages from old mice stimulated lower levels of T cell proliferation than macrophages from young mice. 47,48 This may be due to decreased expression of MHC class II levels on aged macrophages, 49 which contrasts to the stable expression of MHC class II on young and old DCs. 50 Phagocytosis and clearance of infectious organisms are reduced with advanced age.…”

Section: Effect Of Aging On Macrophagesmentioning

confidence: 99%

Effect of Senescence on Macrophage Polarization and Angiogenesis

Dace

Apte

2008

Rejuvenation Research

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There is mounting evidence that as the immune system ages, a progressive deterioration in normal function occurs. Termed immunosenescence, aging impacts both the innate and adaptive immune responses. This review discusses the age-related alterations in the innate immune system, with a specific focus on macrophages. The downstream effect of altered macrophage function on aberrant angiogenesis in the pathophysiology of age-related eye disease is also discussed. 177

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Impaired Antigen Presenting Function of Macrophages from Aged Mice

Abstract: Using antigen-induced proliferation assay the presence of macrophages was found to be essential for the development of the T cell response. Decreased ability of antigen presentation by macrophages from aged A/J mice was detected.

Cited by 33 publications

References 19 publications

The Sex Steroid Precursor DHEA Accelerates Cutaneous Wound Healing Via the Estrogen Receptors

The Sex Steroid Precursor DHEA Accelerates Cutaneous Wound Healing Via the Estrogen Receptors

Accessory Function and Properties of Monocytes from Healthy Elderly Humans for T Lymphocyte Responses to Mitogen and Antigen

Effect of Senescence on Macrophage Polarization and Angiogenesis

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