In vivo immunologic intervention in age-related T cell defects in murine gut-associated lymphoid tissues by IL2

Ajitsu, Shin; Mirabella, Scott; Kawanishi, Hidenori

doi:10.1016/0047-6374(90)90063-l

Cited by 13 publications

(6 citation statements)

References 36 publications

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“…la-c). The observed effects of enteric immunization alone and with I L 2 administration in aged and young adult mice were similar to those obtained in previous reports [7,15]. Again, immune intervention had no significant effect on Ig production by the co-cultured B cells from young adult mice.…”

Section: Antigen-specific Antibody Production In Vitro By Aged/young supporting

confidence: 92%

“…IL 2 synthesis and production are considerably reduced with aging [28,29], and have been found to decline 170-fold in mice from 3 to 22 months of age [23]. Injecting aged mice with (exogenous) IL 2 does not fully remediate the age-related alterations in immune responses of both GALT and non-GALT; as reported previously, the use of IL 2 alone can restore T cell activity to nearly two thirds of the level observed in young adult mice [7]. The decline in helper activity that occurs from 3 to 22 months is only 4-fold [23].…”

Section: Discussionmentioning

confidence: 66%

“…The altered response is due, at least in part, to impaired Ag-specific T, cells. This age-associated hyperresponsiveness can be largely, but not entirely, corrected by in vivo IL 2 administration [7]. Furthermore, we have shown that this in vivo restoration of IL 2 administration is partly due to restoration of the function of the CDW suppressoreffector T cell, thereby ameliorating the aging-associated hyperreactivity toward enteric mycobacterial antigen [7].…”

Section: Introductionmentioning

confidence: 96%

“…Our recent studies [7] have demonstrated hyperreactive gut mucosal humoral immunity to mycobacterial Ag in aged mice. The altered response is due, at least in part, to impaired Ag-specific T, cells.…”

Section: Introductionmentioning

confidence: 98%

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Correction of antigen‐specific T cell defects in aged murine gut‐associated lymphoid tissues an immune intervention by combined adoptive transfer of an antigen‐specific immunoregulatory CD4 T cell subset and interleukin 2 administration

Kawanishi

Ajitsu

1991

Eur J Immunol

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Gut-associated lymphoid tissues (GALT) from aged mice enterically immunized with Mycobacterium paratuberculosis protoplasmic antigen show hyperreactive humoral immune responses; this hyperresponsiveness can be corrected to a considerable extent, but not entirely, by systemic administration of interleukin 2 (IL 2) alone. The aim of the present study was to determine further whether the hyperreactivity in the antigen-specific humoral immune responses in aged GALT could be fully restored by adoptive transfer of in vitro expanded antigen-specific IL 2-dependent helper (CD4+VV-) T cells from GALT in conjunction with recombinant IL 2 administration. The results show that the age-associated hyperresponsiveness in gut mucosal antigen-specific humoral immune responses can be entirely corrected by adoptive transfer with the antigen-specific GALT T helper cells together with in vivo IL 2 administration. The mechanism of this restoration involves reversal of the decline in antigen-specific CD8+ suppressor T cell functions in aged GALT.

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Section: Antigen-specific Antibody Production In Vitro By Aged/young supporting

confidence: 92%

Section: Discussionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 98%

See 2 more Smart Citations

Correction of antigen‐specific T cell defects in aged murine gut‐associated lymphoid tissues an immune intervention by combined adoptive transfer of an antigen‐specific immunoregulatory CD4 T cell subset and interleukin 2 administration

Kawanishi

Ajitsu

1991

Eur J Immunol

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“…28,[98][99][100][101][102] Additional experiments suggest that the picture might be more complex, with defects in production of or sensitivity to IL-2 varying with the activation signal. 5,103 Some investigators have found no difference in T-cell proliferation or IL-2 production when memory T cells from old and young humans were stimulated with a variety of activating signals. 5 CD4+ T cells from old mice accumulate similar levels of IL-2 transcripts, though secretion of IL-2 is lower than in cells from young mice.…”

Section: Interleukinsmentioning

confidence: 99%

Aging, Immunity, and Cancer

Burns

Leventhal

2000

Cancer Control

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Antiaging Agent

Jolley¹,

Cottam²

2000

Kirk-Othmer Encyclopedia of Chemical Technology

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The human aging process is extremely complex and appears to affect all bodily functions equally. The tremendous advances in molecular biology over the past decade have made it possible to begin to study the basic mechanisms of aging at the molecular level and relate those findings to specific age‐related diseases at the cellular, tissue, and organ level. It is likely that these advances will demonstrate that there are multiple mechanisms underlying the aging process at all levels and that multiple interventions will therefore be necessary to arrest, slow, or reverse the aging process. Factors already known to be intimately involved in aging include environmental, dietary, and genetic influences; each appears to be involved. Consequently, no single agent is likely to be found that will arrest or reverse all aging processes. Current research efforts focus mostly on modulation of single aging processes and on one or two major organ systems of the body. It is essential to distinguish intrinsic aging from age‐dependent abnormalities, eg, in the cumulative assault of sunlight on the skin. Sunscreens block the cutaneous absorption of ultraviolet (uv) light radiation (280–315 nm) and prevent sunburning, premature aging, and cancer of the skin. Photoaged skin, long believed to be irreversibly damaged, has now been shown to undergo significant repair when uv exposures are stopped. Aging is associated with progressive deterioration in CNS function. A number of factors besides genetic considerations contribute to those degenerative changes, including nutritional elements and environmental toxins. The blood brain barrier (BBB) is a major modulator of nutrient delivery to the CNS. Senescence is associated with significant changes in BBB function including a decrease in BBB choline transport and brain glucose influx. Studies have confirmed that enhancing the cholinergic system could lead to reversal of age‐related memory loss. Evidence indicating an activation of cholinergic mechanisms exists for pyrrolidinone derivatives, including piracetam, oxiracetam, aniracetam, pyroglutamic acid, tenilsetam, and pramiracetam, and for vinpocetine, naloxone, ebiratide, and phosphatidylserine. All these drugs prevent disruptions of several learning and memory paradigms. Cardiovascular disease remains the most common age‐related disease and is the most common cause of morbidity and mortality in old age. Risk factors more prevalent in the elderly than in the young adult, that initiate and aggravate cardiovascular disease include hypertension, personality traits, genetics, diet, smoking, obesity, and impaired glucose tolerance. Pharmacological agents such as lovastatin are used for the treatment of hypercholesterolemia, and antiatherosclerogenic diets low in saturated fat and cholesterol, rich in fiber, and with substitution of polyunsaturated fat and restricted calories tend to normalize serum lipids and to cause lesions to involute. One important feature of aging is the remodeling of the ventricle and blood vasculature. Various agents such as vasodilators, hydroalazine, and isosorbide dinitrate have been used. Other possibilities include α‐blockers and calcium antagonists. Normal aging is associated with a gradual decline in the immune response. A number of approaches have been devised to prevent the loss of immune responsiveness or to restore it once it is declining or has been lost. Recovery of T‐regulatory effects on B‐cell differentiation has been reported in elderly patients treated with IL‐1 or IL‐2. Levamisole, C 11 H 12 N 2 S, and the sodium salt of diethyl dithiocarbamate (imuthiol) restore T‐cell function. Hypoxanthine derivatives such as isoprinosine and NPT 15392 induce T‐cell maturation directly and promote T‐cell function. Melatonin, the pineal neurohormone N ‐acetyl‐5‐methoxytryptamine, has been shown to antagonize the immunosuppressive effects of anxiety stress in mice. The 8‐substituted guanosines have been found to stimulate nonspecific, as well as some specific immune responses. The transmembrane signaling component of cellular activation has been an area of intense research interest. The interactions between nutrition and immunity have been the subject of much investigation. It is now recognized that even mild deficiencies involving protein–calorie malnutrition or single nutrients are associated with impaired immune responses. Large doses of “essential” nutrients (eg, zinc) may have a deleterious effect on the immune system. However, corrections of deficiencies of iron, zinc, and vitamins C, E, and B complex are associated with improved immune responses in the elderly.

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In vivo immunologic intervention in age-related T cell defects in murine gut-associated lymphoid tissues by IL2

Cited by 13 publications

References 36 publications

Correction of antigen‐specific T cell defects in aged murine gut‐associated lymphoid tissues an immune intervention by combined adoptive transfer of an antigen‐specific immunoregulatory CD4 T cell subset and interleukin 2 administration

Correction of antigen‐specific T cell defects in aged murine gut‐associated lymphoid tissues an immune intervention by combined adoptive transfer of an antigen‐specific immunoregulatory CD4 T cell subset and interleukin 2 administration

Aging, Immunity, and Cancer

Antiaging Agent

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