Differences in effect of isoproterenol stimulation on levels of cyclic AMP in human B and T lymphocytes

Niaudet, Patrick; Beaurain, Geneviève; Bach, Marie‐Anne

doi:10.1002/eji.1830061117

Cited by 54 publications

(10 citation statements)

References 18 publications

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“…These observations may further support the nonrandom nature of the distribution of receptors for autacoids on T cell subsets. The selectivity in the responsiveness of different populations of T cells to beta adrenergic agonists and histamine had earlier been reported (17)(18)(19). Corticosteroid resistant murine thymocytes were less responsive to isoproterenol than untreated thymocytes.…”

Section: Resultssupporting

confidence: 53%

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Pharmacologic effects of autacoids on subsets of T cells. Regulation of expression/function of histamine-2 receptors by a subset of suppressor cells.

Khan¹,

Sansoni²,

Engleman³

et al. 1985

J. Clin. Invest.

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Section: Resultssupporting

confidence: 53%

“…The latter were more responsive than lymphoid cells from spleen, lymph node, and blood (17). Niaudet et al (19) reported that T lymphocytes isolated from human peripheral blood produced more cAMP in response to isoproterenol than T cells isolated from human tonsils and adenoids.…”

Section: Resultsmentioning

confidence: 99%

Pharmacologic effects of autacoids on subsets of T cells. Regulation of expression/function of histamine-2 receptors by a subset of suppressor cells.

Khan¹,

Sansoni²,

Engleman³

et al. 1985

J. Clin. Invest.

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“…In contrast, mature corticosterone-resistant thymocytes were demonstrated to express ␤ -AR at levels equivalent to those seen in peripheral T cells [123,131] . Despite the differential level of expression on immature and mature thymocytes, the efficiency of ␤ -AR coupling to adenylate cyclase in unfractionated thymocytes and mature thymocytes was comparable to that seen in lymphocytes from spleen and lymph nodes [132] . Further, unfractionated thymocytes were shown to generate an isoproterenol-induced cAMP response that is equivalent to that in splenocytes, even though splenocytes express a far greater number of ␤ -ARs [133] .…”

Section: Expression Of Ars In the Thymusmentioning

confidence: 99%

Age-Associated Remodeling of Neural and Nonneural Thymic Catecholaminergic Network Affects Thymopoietic Productivity

Leposavić

Pilipović

Perišić

2011

Neuroimmunomodulation

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Ageing is associated with a progressive decline in thymic cytoarchitecture followed by a less efficient T cell development and decreased emigration of naïve T cells to the periphery. These thymic changes are linked to increased morbidity and mortality from infectious, malignant and autoimmune diseases in old age. Therefore, it is of paramount importance to understand the thymic homeostatic processes across the life span, as well as to identify factors and elucidate mechanisms driving or contributing to the thymic involution. Catecholamines (CAs) derived from sympathetic nerves and produced locally by thymic cells represent an important component of the thymic microenvironment. In young rats, they provide a subtle tonic suppressive influence on T cell development acting via β₂- and α₁-adrenoceptors (ARs) expressed on thymic nonlymphoid cells and thymocytes. In the face of thymic involution, a progressive increase in the thymic noradrenaline level, reflecting a rise in the density of noradrenergic nerve fibers and CA-synthesizing cells, occurs. In addition, the density of β₂- and α₁-AR-expressing thymic nonlymphoid cells and the α₁-AR thymocyte surface density also exhibit a pronounced increase with age. The data obtained from studies investigating effects of AR blockade on T cell development indicated that age-related changes in CA-mediated thymic communications, certainly those involving α₁-ARs, may contribute to diminished thymopoietic efficiency in the elderly. Having in mind thymic plasticity in the course of ageing, and broadening possibilities for pharmacological modulation of CA signaling, we here present and discuss the progress in research related to a role of CAs in thymic homeostasis and age-related decay in the thymic naïve T cell output.

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“…Because it is difficult to study samples of lung in human subjects, several investigators have used either peripheral blood leukocytes or lymphocytes to show that asthmatics have decreased stimulation of cyclic AMP by beta adrenergic agonists (7,8). Two problems must be considered in assessing these studies: (a) beta adrenergic responses and receptors in T and B lymphocytes may be quite different (9,10), and thus changes in adrenergic response in asthmatics might reflect altered distribution of cells in lymphocyte subpopulations; and (b) prior administration of beta adrenergic agonists reportedly diminishes subsequent beta adrenergic stimulation of leukocyte cyclic AMP (11)(12)(13). Thus, changes in responsiveness of asthmatics might arise from therapy as well as from the disease itself.…”

Section: Introductionmentioning

confidence: 99%

Beta Adrenergic Receptors of Polymorphonuclear Particulates in Bronchial Asthma

Galant¹,

Duriseti²,

Underwood³

et al. 1980

J. Clin. Invest.

105

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A B S T R A C T We have tested the beta adrenergic receptor theory of bronchial asthma by determining the number and affinity of binding sites of the beta adrenergic radioligand [3H]dihydroalprenolol (DHA) and the activity ofadenylate cyclase in broken cell preparations of polymorphonuclear leukocytes (PMN). We studied 31 control subjects (group 1), 30 asthmatics receiving no systemic adrenergic medication (group 2), and 17 asthmatics receiving adrenergic agonists systemically (group 3). Control subjects and asthmatics taking no adrenergic drugs bound similar amounts of DHA at 0.5 nM and 30 nM DHA and had about 900 binding sites per PMN. In contrast, asthmatics receiving adrenergic agonists had a >70% decrease in their number of DHA binding sites per PMN (254+±57). In a subset of our three groups of subjects (eight from group 1, six from group 2, and five from group 3) we measured DHA binding at several DHA concentrations and found similar values (0.4-0.7 nM) for the dissociation constant of DHA among these subjects.In further studies we examined the interaction of the agonist (-)-isoproterenol with beta adrenergic receptors in 8 normal subjects and 10 asthmatics not receiving adrenergic medication. We tested the ability of isoproterenol to compete for DHA binding sites and to stimulate adenylate cyclase in sonicates prepared from PMN and examined under identical conditions. The dissociation constants for the competition of isoproterenol for DHA binding sites in normal and asthmatic subjects were virtually identical (-1.0,M). In addi-

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Differences in effect of isoproterenol stimulation on levels of cyclic AMP in human B and T lymphocytes

Cited by 54 publications

References 18 publications

Pharmacologic effects of autacoids on subsets of T cells. Regulation of expression/function of histamine-2 receptors by a subset of suppressor cells.

Pharmacologic effects of autacoids on subsets of T cells. Regulation of expression/function of histamine-2 receptors by a subset of suppressor cells.

Age-Associated Remodeling of Neural and Nonneural Thymic Catecholaminergic Network Affects Thymopoietic Productivity

Beta Adrenergic Receptors of Polymorphonuclear Particulates in Bronchial Asthma

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