Antigen-dependent increase in cytosolic free calcium in specific human T-lymphocyte clones

Nisbet-Brown, Eric; Cheung, Roy K.; Lee, J. W. W.; Gelfand, Erwin W.

doi:10.1038/316545a0

Cited by 90 publications

(26 citation statements)

References 23 publications

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“…Special attention has been focused on the endoplasmic reticulum (ER) of activated and resting T lymphocytes. This intracellular membranebound system is in fact known to include the rapidly exchanging Ca2+ store, sensitive to the second messenger inositol 1,4,5-trisphosphate (IP3), and to be responsible for the [Ca2+]i increase induced by receptor signaling [4][5][6][7]101. The results obtained demonstrate that during in vitro and in vivo T lymphocyte activation the distribution of Ca2+ within the cell is profoundly modified.…”

Section: Introductionmentioning

confidence: 99%

Intracellular Ca²⁺ stores of T lymphocytes: Changes induced by in vitro and in vivo activation

et al. 1994

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Intracellular Ca2+ stores were investigated in resting and activated splenic T lymphocytes from Lewis rats. Activation was obtained either in vitro (spleen cells isolated from "naive" rats exposed to concanavalin A for 24 h) or in vivo (spleen cells from rats with fully developed symptoms of experimental allergic encephalomyelitis). In both experimental conditions several changes of Ca2+ homeostasis were observed with respect to resting lymphocytes: (1) a threefold increase of the total intracellular calcium (from 1.15 to 3.5 mmol/l); (2) a moderate increase of the pool sensitive to inositol 1,4,5-trisphosphate (IP3), investigated both in intact T lymphocytes (fura-2 and 45Ca(2+)-release techniques in cells challenged with phytohemagglutinin) and in T lymphocytes permeabilized with beta-escin (45Ca2+ release induced by saturating concentrations of IP3); and (3) the appearance of a pool released by the endoplasmic reticulum (ER) Ca2+ ATPase inhibitor thapsigargin (Tg), but insensitive to IP3, which, therefore, appears to be localized in areas of the ER devoid of the cognate receptor. The latter two findings were paralleled in activated lymphocytes by an increase of expression of ER markers, involved (calreticulin; Ca2+ ATPase) or not (protein disulfide isomerase) in the regulation of Ca2+ homeostasis. In contrast, calnexin (another ER marker) and the receptor for IP3 were increased to only a moderate extent. Finally, an enlargement of non-ER Ca2+ pools was observed in the cells pretreated with Tg in which 45Ca2+ release was induced by the Ca2+ ionophore ionomycin. Our results document structural and functional changes of intracellular Ca2+ stores which might play an important regulatory role in activated T lymphocytes.

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Section: Introductionmentioning

confidence: 99%

Intracellular Ca²⁺ stores of T lymphocytes: Changes induced by in vitro and in vivo activation

et al. 1994

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“…A role for cytoplasmic Ca2' in T lymphocyte mitogenesis was originally suggested by the requirement for extracellular Ca" ([Ca2'],) in proliferation [l, 21 and by the mitogenic effect of the divalent cation ionophore A23187 [3, 41. Changes in plasma membrane permeability to Ca" in response to mitogens were first inferred from measurements of 45Ca2+ fluxes and distribution [5- [15], by specific antigen presented by DR-compatible, antigen-presenting cells [17], or by antibodies to T11 [18], the sheep erythrocyte binding protein.…”

Section: Introductionmentioning

confidence: 99%

Uptake of extracellular Ca²⁺ and not recruitment from internal stores is essential for T lymphocyte proliferation

et al. 1988

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Changes in free cytosolic calcium concentrations ([Ca2+]i) are thought to be important initiating events in the activation of T lymphocytes. Mitogen-induced increases in [Ca2+]i may result from net influx across the plasma membrane and/or release of Ca2+ from intracellular stores. In human T lymphocytes loaded with the fluorescent indicator indo-1, addition of phytohemagglutinin (PHA) or the anti-CD3 antibody UCHT-1 elicits a biphasic [Ca2+]i response. A major component of the initial transient peak was due to release from internal stores whereas the lower plateau phase was sustained by Ca2+ influx. Previous work suggested that Ca2+ influx is essential for interleukin 2 (IL 2) secretion and cell proliferation. To determine the relative effects of the initial and sustained phases of [Ca2+]i change, IL 2 secretion and cell proliferation, we introduced into the cell 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), a high affinity intracellular Ca2+ chelator which neither contributes to nor interferes with the fluorescence determinations of [Ca2+]i. In cells preloaded with BAPTA, both PHA and UCHT-1 antibody failed to elicit the transient [Ca2+]i overshoot. Only the plateau phase could be observed in the presence of extracellular Ca2+. In contrast, BAPTA-loaded cells were found to be fully functional when assessed for IL 2 receptor expression, IL 2 secretion and cell proliferation. Thus, the mitogen-induced, maximal but transient increase in [Ca2+]i, contributed to mainly by release of Ca2+ from internal stores, does not appear to be essential for these T cell responses.

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“…ALDO and extracellular Na ϩ are each known to upregulate Ca 2ϩ uptake in various cells, including lymphocytes. 70 83 It has been reported to play a major regulatory role in the generation of reactive oxygen species in chemotactic factor-stimulated neutrophils. 81 Concordant with the rise in intracellular Ca 2ϩ was the induction of oxidative/nitrosative stress in PBMCs, as indicated by several lines of evidence.…”

Section: Ahokas Et Al Aldosteronism and Pbmcsmentioning

confidence: 99%

Aldosteronism and Peripheral Blood Mononuclear Cell Activation

Ahokas

Warrington

Gerling

et al. 2003

Circulation Research

118

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Abstract-Aldosteronism eventuates in a proinflammatory/fibrogenic vascular phenotype of the heart and systemic organs.It remains uncertain whether peripheral blood mononuclear cells (PBMCs) are activated before tissue invasion by monocytes/macrophages and lymphocytes, as is the case for responsible pathogenic mechanisms. Uninephrectomized rats treated for 4 weeks with dietary 1% NaCl and aldosterone (ALDOST, 0.75 g/h) with or without spironolactone (Spi, 100 mg/kg per daily gavage) were compared with unoperated/untreated and uninephrectomized/salt-treated controls. Before intramural coronary vascular lesions appeared at week 4 of ALDOST, we found (1) a reduction of PBMC cytosolic free [Mg 2ϩ ] i , together with intracellular Mg 2ϩ and Ca 2ϩ loading, whereas plasma and cardiac tissue Mg 2ϩ were no different from controls; (2) increased H 2 O 2 production by monocytes and lymphocytes together with upregulated PBMC gene expression of oxidative stress-inducible tyrosine phosphatase and Mn 2ϩ -superoxide dismutase and the presence of 3-nitrotyrosine in CD4ϩ and ED-1-positive inflammatory cells that had invaded intramural coronary arteries; (3) B-cell activation, including transcription of immunoglobulins, intracellular adhesion molecule-1, and CC and CXC chemokines and their receptors; (4) expansion of B lymphocyte subset and myosin heavy chain class II-expressing lymphocytes; and (5) autoreactivity with gene expression for antibodies to acetylcholine receptors and a downregulation of RT-6.2, which is in keeping with cell activation and associated with autoimmunity. Spi cotreatment attenuated the rise in intracellular Ca 2ϩ , the appearance of oxidative/nitrosative stress in PBMCs and invading inflammatory cells, and alterations in PBMC transcriptome. Thus, aldosteronism is associated with an activation of circulating immune cells induced by iterations in PBMC divalent cations and transduced by oxidative/nitrosative stress. ALDO receptor antagonism modulates this neuroendocrine-immune interface. The full text of this article is available online at http://www.circresaha.org. (Circ Res. 2003;93:e124-e135.) Key Words: aldosterone Ⅲ peripheral blood mononuclear cells Ⅲ hydrogen peroxide production Ⅲ cytosolic free Mg 2ϩ and Ca 2ϩ Ⅲ transcriptome I rrespective of its etiologic origins, asymptomatic ventricular systolic dysfunction eventuates in an activation of the circulating renin-angiotensin-aldosterone system (RAAS), whose effector hormones contribute to the appearance of the congestive heart failure (CHF) syndrome. A chronic systemic illness ensues that features oxidative/nitrosative stress in such diverse tissues as skeletal muscle, peripheral blood mononuclear cells (PBMCs) (monocytes and lymphocytes), and heart 1-11 ; elevated circulating levels of proinflammatory cytokines and chemokines [12][13][14][15][16][17][18][19][20][21] ; and a wasting syndrome that eventuates in cachexia. 22 Pharmacological modulation of RAAS effector hormones has proven clinical benefits in patients with CHF. [23][24][25][26][27] A ro...

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Antigen-dependent increase in cytosolic free calcium in specific human T-lymphocyte clones

Cited by 90 publications

References 23 publications

Intracellular Ca²⁺ stores of T lymphocytes: Changes induced by in vitro and in vivo activation

Intracellular Ca²⁺ stores of T lymphocytes: Changes induced by in vitro and in vivo activation

Uptake of extracellular Ca²⁺ and not recruitment from internal stores is essential for T lymphocyte proliferation

Aldosteronism and Peripheral Blood Mononuclear Cell Activation

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Antigen-dependent increase in cytosolic free calcium in specific human T-lymphocyte clones

Cited by 90 publications

References 23 publications

Intracellular Ca2+ stores of T lymphocytes: Changes induced by in vitro and in vivo activation

Intracellular Ca2+ stores of T lymphocytes: Changes induced by in vitro and in vivo activation

Uptake of extracellular Ca2+ and not recruitment from internal stores is essential for T lymphocyte proliferation

Aldosteronism and Peripheral Blood Mononuclear Cell Activation

Contact Info

Product

Resources

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Intracellular Ca²⁺ stores of T lymphocytes: Changes induced by in vitro and in vivo activation

Intracellular Ca²⁺ stores of T lymphocytes: Changes induced by in vitro and in vivo activation

Uptake of extracellular Ca²⁺ and not recruitment from internal stores is essential for T lymphocyte proliferation