Interleukin-2-dependent T lymphocytes for the diagnosis and investigation of inherited metabolic disorders

Adolph, Kelvin; Kucey, Mark T.; Hodges, Stephen D.; Carter, Robert J.; Snyder, Floyd F.

doi:10.1016/0009-8981(88)90252-5

Cited by 8 publications

(3 citation statements)

References 21 publications

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“…Heparinized blood was transported and stored at ambient room temperature for up to 48 h prior to further processing. Lymphocytes were isolated from 2.2 ml of blood and IL-2-dependent T lymphocytes cultured as described (Adolph et al 1988). Cells were harvested by centrifugation after 12-14 days of culture and the cell pellets stored at -30°C.…”

Section: Methodsmentioning

confidence: 99%

Carrier detection in glutaric aciduria type I using interleukin‐2‐dependent cultured lymphocytes

Seargeant

Chudley

Dilling

et al. 1992

J of Inher Metab Disea

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Cultured interleukin 2 (IL-2)-dependent leukocytes from 13 patients with glutaric aciduria type I, 12 obligate carriers, 105 family members and 31 normal controls were assayed for glutaryl-CoA dehydrogenase activity. Of the 13 affected patients, 10 (all Ojibway Indian) had residual enzyme activity (2-13% of control) and 3 patients (all non-Indian) had undetectable enzyme activity. There was partial overlap between the distribution of enzyme activity in obligate heterozygotes and in normal controls (mean values +/- SD: 6.29 +/- 0.94 and 10.75 +/- 2.58 nmol/h per mg protein respectively). Using an arbitrary cutoff level of < 7 nmol/h per mg protein as presumptive evidence of carrier status, the observed frequency of carriers did not differ significantly from that expected from their a priori risk of carrier status. Thirteen per cent of the family members had inconclusive status (activity between 7 and 8.5 nmol/h per mg protein). The method appears suitable for carrier detection, although definitive carrier assignment awaits identification of the mutation(s) responsible for glutaric aciduria type I.

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Section: Methodsmentioning

confidence: 99%

Carrier detection in glutaric aciduria type I using interleukin‐2‐dependent cultured lymphocytes

Seargeant

Chudley

Dilling

et al. 1992

J of Inher Metab Disea

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“…Lymphocytes were isolated from whole blood using LeucoPrep tubes (BectonDickenson), then placed in culture (RPMI 1640, containing phytohemaglutinin, interleukin-2, and catalase) for a period of one to three weeks to achieve an eightfold expansion of cell number (Adolph et al 1988). Prior to binding assays, cells were harvested, washed once in phosphate buffered saline containing 25 mM HEPES and preincubated for 15 min at 25 Њ C with inhibitors of proteolysis (bestatin, aprotinin, PMSF) in 50 mM TrisCl, pH 7.4, containing 0.1 mg/ml bovine serum albumin and 10 mM magnesium chloride.…”

Section: Lymphocyte Binding Assaymentioning

confidence: 99%

Aging and Panicogenic Response to Cholecystokinin Tetrapeptide An Examination of the Cholecystokinin System

Flint

Bradwejn

Vaccarino

et al. 2002

Neuropsychopharmacology

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Older age is associated with diminished symptomatic and cardiovascular response to the panicogenic agent cholecystokinin tetrapeptide (CCK-4). We hypothesized that circulating concentrations of endogenous CCK-4 and/or CCK-8 are increased in later life, possibly due to decreased enzymatic degradation, and that this is associated with desensitization of CCK-B receptors. The study group consisted of 20 healthy subjects aged 18-30 years and 20 healthy subjects aged years. The two groups were compared on fasting basal plasma concentrations of and nonsulfated , and on binding capacity of lymphocyte CCK-B receptors. Under single-blind (to subject) conditions, subjects were then administered an intravenous bolus of placebo, followed 50 min later by an intravenous bolus of 50 g of Cholecystokinin (CCK) is a gastrin-like peptide with several molecular forms, ranging from 4 to 58 amino acid residues (Crawley and Corwin 1994). CCK was first isolated from the alimentary tract, where it has an important role in stimulating gallbladder contraction and the release of pancreatic enzymes. CCK is also abundant in the brain, where it functions as both a neurotransmitter and a neuromodulator. Two types of CCK receptor have been identified: CCK-A receptors, which are found in the viscera and some distinct brain regions, and CCK-B receptors, which are predomi- NO . 4 nantly located and widely distributed in the brain (Crawley and Corwin 1994).Intravenous administration of cholecystokinin tetrapeptide (CCK-4), a selective CCK-B agonist, produces panic attacks in humans (Bradwejn 1993). The mechanism of CCK-4-induced panic is not known. However, animal and clinical work suggests that brainstem CCK-B receptors may mediate the panicogenic effects of CCK-4, possibly through direct or indirect interaction with other neurotransmitter systems (Bradwejn 1993). Prompted by epidemiologic evidence that the prevalence and incidence of panic disorder decline in later life (Flint et al. 1996), we previously investigated the effect of aging on healthy subjects' response to CCK-4. We found that older subjects had significantly fewer and less intense symptoms of panic, shorter duration of symptoms, and less autonomic reactivity to CCK-4 compared with younger subjects (Flint et al. 1998). The purpose of the current study was to determine whether there are age-related changes in the CCK system that could account for older subjects' attenuated response to CCK-4.Studies in animals and humans have consistently found an age-related decline in sensitivity of the gallbladder and pancreas to CCK (Khalil et al. 1984(Khalil et al. , 1985a Kitani 1987, 1989;Masclee et al. 1988;Poston et al. 1988aPoston et al. , 1990Ishizuka et al. 1993). Furthermore, animal studies have found that aging is associated with a reduction in the mRNA level of pancreatic CCK-A receptors (Miyasaka et al. 1995a) and a decreased density of CCK receptors in the pancreas and gallbladder (Poston et al. 1988a,b). Very little is known about the effect of aging on brain CCK, and to our k...

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“…In a recent study, a panel of 19 enzymes was assayed in IL-2-dependent T-lymphocytes, and the diagnosis of four enzyme deficiencies was demonstrated (Adolph et al, 1988). However, the activity of the enzymes in IL-2-dependent T-cells and in noncultured cells was not compared.…”

Section: Introductionmentioning

confidence: 99%

Arylsulfatase A and β-galactosidase activities in leukocytes and lymphocytes from normal and psychiatric subjects

Shah

Johnson

Minn

et al. 1995

Molecular and Chemical Neuropathology

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Arylsulfatase A (ASA) and cerebroside-beta-galactosidase activities in leukocytes serve as a diagnostic tool for determining the presence of metachromatic leukodystrophy and globoid cell leukodystrophy, respectively. It has not been demonstrated whether a delay in blood processing and the presence of mixed cell types in different proportions in leukocytes affect the activities of the two enzymes in these cells. We have in the present study determined the specific activity in leukocytes and lymphocytes (T-cells) prepared from blood samples processed immediately after, 4, and 24 h after collection. In order to determine whether the enzyme activities in lymphocytes reflect expression of genetic trait, and not environmental or "state" influence, the activities of the two enzymes in interleukin 2-stimulated T-cells and resting T-cells were compared. A delay of up to 24 h in blood processing did not significantly change the specific activities of the two enzymes in both leukocytes and lymphocytes. The specific activity of ASA and beta-galactosidase in lymphocytes was 1.4-1.8 times that in leukocytes. The activities of the two enzymes in interleukin 2-stimulated T-cells did not differ from those in resting T-cells. These results indicate that blood-processing delay had no significant effects on ASA and beta-galactosidase activity. The data further indicate that the ASA and beta-galactosidase activity in interleukin 2-stimulated T-cells was not significantly different from resting lymphocytes from either normal or psychiatric subjects exposed to various medications. The activity levels in lymphocytes from psychiatric subjects thus reflect expression of genetic trait, rather than environmental or state influence.

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Interleukin-2-dependent T lymphocytes for the diagnosis and investigation of inherited metabolic disorders

Cited by 8 publications

References 21 publications

Carrier detection in glutaric aciduria type I using interleukin‐2‐dependent cultured lymphocytes

Carrier detection in glutaric aciduria type I using interleukin‐2‐dependent cultured lymphocytes

Aging and Panicogenic Response to Cholecystokinin Tetrapeptide An Examination of the Cholecystokinin System

Arylsulfatase A and β-galactosidase activities in leukocytes and lymphocytes from normal and psychiatric subjects

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