Measurement ofCandida-specific blastogenesis: Comparison of carboxyfluorescein succinimidyl ester labelling of T cells, thymidine incorporation, and CD69 expression

Angulo, Rudy; Fulcher, DA

doi:10.1002/(sici)1097-0320(19980615)34:3<143::aid-cyto4>3.0.co;2-i

Cited by 86 publications

(24 citation statements)

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“…The proliferative index was calculated from the data in the histograms considering that two cells with a given CFSE intensity were produced by mitosis of a single cell, possessing a CFSE intensity immediately above, using the following formula (17): proliferative index = (100-Y)/Y, where Y (%) = X0+X1/2+X2/4+X3/8+X4/16+X5/32+X6/64+X7/128, X0 represents the percentage of T cells that did not divide (located at M1), and X1-7 represents the peak of gradual division (located from M2 to M7).…”

Section: Methodsmentioning

confidence: 99%

Leukocytosis, muscle damage and increased lymphocyte proliferative response after an adventure sprint race

Tossige-Gomes

Ottone

Oliveira

et al. 2014

Braz J Med Biol Res

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The effect of an adventure sprint race (ASR) on T-cell proliferation, leukocyte count and muscle damage was evaluated. Seven young male runners completed an ASR in the region of Serra do Espinhaço, Brazil. The race induced a strong leukocytosis (6.22±2.04×103 cells/mm3 before vs 14.81±3.53×103 cells/mm3 after the race), marked by a significant increase of neutrophils and monocytes (P<0.05), but not total lymphocytes, CD3+CD4+ or CD3+CD8+ cells. However, the T-cell proliferative response to mitogenic stimulation was increased (P=0.025) after the race, which contradicted our hypothesis that ASR, as a high-demand competition, would inhibit T-cell proliferation. A positive correlation (P=0.03, r=0.79) was observed between the proliferative response of lymphocytes after the race and the time to complete the race, suggesting that the proliferative response was dependent on exercise intensity. Muscle damage was evident after the race by increased serum levels of aspartate amino transferase (24.99±8.30 vs 50.61±15.76 U/L, P=0.003). The results suggest that humoral factors and substances released by damaged muscle may be responsible for lymphocyte activation, which may be involved in muscle recovery and repair.

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Section: Methodsmentioning

confidence: 99%

Leukocytosis, muscle damage and increased lymphocyte proliferative response after an adventure sprint race

Tossige-Gomes

Ottone

Oliveira

et al. 2014

Braz J Med Biol Res

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“…The division index ϭ (100ϪY)/Y, where Y (%) ϭ x 0 ϩ x 1 /2 ϩ x 2 /4 ϩ x 3 /8 ϩ x 4 /16 ϩ x 5 /32 ϩ x 6 /64 ϩ x 7 /128 and x 0 represents the percentage of B cells that have not divided. 12 …”

Section: Proliferation Assay and Mitotic Indexmentioning

confidence: 99%

TC-PTP–deficient bone marrow stromal cells fail to support normal B lymphopoiesis due to abnormal secretion of interferon-γ

Bourdeau

Dubé

Heinonen

et al. 2007

Blood

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The T-cell protein tyrosine phosphatase (TC-PTP) is a negative regulator of the Jak/Stat cytokine signaling pathway. Our study shows that the absence of TC-PTP leads to an early bone marrow B-cell deficiency characterized by hindered transition from the pre-B cell to immature B-cell stage. This phenotype is intrinsic to the B cells but most importantly due to bone marrow stroma abnormalities. We found that bone marrow stromal cells from TC-PTP ؊ IntroductionThe T-cell protein tyrosine phosphatase (TC-PTP) is an intracellular enzyme encoded by Ptpn2. It is ubiquitously expressed, with highest levels in hematopoietic tissues (for a review, see Bourdeau et al 1 ). TC-PTP Ϫ/Ϫ mice appear physically normal until 10 to 14 days of age, at which time they progressively develop tissue mononuclear cell infiltrates. 2 Elevated levels of IFN-␥ can be measured at 19 days of age, 3 and the animals die between 21 and 35 days of age. TC-PTP Ϫ/Ϫ mice display defective hematopoiesis and immune function, characterized by anemia and splenomegaly secondary to sequestration of erythrocytes and accumulation of myeloid cells. 2 TC-PTP was also shown to interact with TRAF2 downstream of the TNF proinflammatory cytokine. This interaction inactivated Src and suppressed MAPK signaling. 4 TC-PTP has been identified as a critical regulator of colony-stimulating factor 1 (CSF-1) signaling and mononuclear phagocyte development. On CSF-1 stimulation, a deficiency in TC-PTP leads to enhanced tyrosine phosphorylation of the Grb2/Gab2/Shp2 complex by the CSF-1 receptor and increased activation of Erk. 5 These results identified TC-PTP as a key modulator of inflammatory signals as well as macrophage and lymphocyte functions.TC-PTP has been shown to control cytokine signaling events by its negative action on the Janus kinase (Jak) and signal transducer and activator of transcription (Stat) pathways (reviewed by Bourdeau et al 1 ). This cascade is crucial for hematopoietic development and cellular response to growth factors. 6 Using an in vitro approach, TC-PTP substrate-trapping mutant D/A was shown to interact with Jak1 and Jak3. 7 Stat1, Stat3, and Stat5a/5b were also identified as substrates for TC-PTP. [8][9][10] It is clear that TC-PTP is a key director of several cytokine-signaling pathways, and thus may be involved in the development of multiple hematopoietic lineages.Here, we report that bone marrow stromal cells from TC-PTP Ϫ/Ϫ mice secrete abnormally high levels of IFN-␥, resulting in constitutive phosphorylation of Stat1 in pre-B cells and altered B-cell development in the bone marrow. Our findings are novel and reflect the therapeutic potential of TC-PTP as a modulator of bone marrow stroma microenvironment that could be exploited in leukemia and other immune disorders. Materials and methods MiceGeneration of TC-PTP mutant mice was described previously. 2 Experiments were performed with mice on a mixed Balb/c-129SJ background and with mice backcrossed for 8 generation on Balb/c. All procedures were approved by the McGill University Rese...

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“…To verify this, we used carboxyfluorescein diacetate succinimidyl ester to trace cell divisions and noted that the PTP-1B Ϫ͞Ϫ cells divided on average one more time than the control cells over the 5-day incubation period as seen by a decrease in fluorescence due to cell division (Fig. 2B) and increased mitotic index (1.4 Ϯ 0.2 for PTP-1B ϩ͞ϩ vs. 2.5 Ϯ 0.6 for PTP-1B Ϫ͞Ϫ; P Ͻ 0.05) (24).…”

Section: Augmented Monocytic But Not Granulocytic Development In Thementioning

confidence: 99%

Protein tyrosine phosphatase 1B negatively regulates macrophage development through CSF-1 signaling

Heinonen

Dubé

Bourdeau

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Protein tyrosine phosphatase 1B (PTP-1B) is a ubiquitously expressed cytosolic phosphatase with the ability to dephosphorylate JAK2 and TYK2, and thereby down-regulate cytokine receptor signaling. Furthermore, PTP-1B levels are up-regulated in certain chronic myelogenous leukemia patients, which points to a potential role for PTP-1B in myeloid development. The results presented here show that the absence of PTP-1B affects murine myelopoiesis by modifying the ratio of monocytes to granulocytes in vivo. This bias toward monocytic development is at least in part due to a decreased threshold of response to CSF-1, because the PTP-1B ؊͞؊ bone marrow presents no abnormalities at the granulocytemonocyte progenitor level but produces significantly more monocytic colonies in the presence of CSF-1. This phenomenon is not due to an increase in receptor levels but rather to enhanced phosphorylation of the activation loop tyrosine. PTP-1B ؊͞؊ cells display increased inflammatory activity in vitro and in vivo through the constitutive up-regulation of activation markers as well as increased sensitivity to endotoxin. Collectively, our data indicate that PTP-1B is an important modulator of myeloid differentiation and macrophage activation in vivo and provide a demonstration of a physiological role for PTP-1B in immune regulation.hematopoiesis ͉ innate immunity ͉ myeloid progenitor cells P rotein tyrosine phosphatase 1B (PTP-1B; also known as PTPN1) is a ubiquitously expressed cytosolic phosphatase that is localized to the endoplasmic reticulum (1). PTP-1B Ϫ͞Ϫ mice were shown to be resistant to diet-induced diabetes and obesity (2-5), and the enzyme has been implicated in several metabolic pathways because of its ability to dephosphorylate and thereby down-regulate the activity of the insulin receptor (2, 3), epidermal growth factor receptor and platelet-derived growth factor receptor (6-8), insulin-like growth factor type I receptor (4, 9), and JAKs associated with cytokine family receptors, including leptin (5, 10) and growth hormone receptors (11). PTP-1B appears to show specificity toward JAK2 and TYK2 (12), and has been shown to regulate IFN signaling in fibroblasts (12). Despite the regulatory role in cytokine signaling, no immunological phenotype has been attributed to the PTP-1B-deficient mice to date.IL-3, granulocyte colony-stimulating factor (G-CSF), and granulocyte-monocyte colony-stimulating factor (GM-CSF) are cytokines that depend on JAK2 activity for signaling (13-15) and play important roles in the regulation of myeloid development (16). The receptor for another important myeloid cytokine, CSF-1, belongs to the class III receptor tyrosine kinase family together with the platelet-derived growth factor receptor (17), and it also activates TYK2 (18). Furthermore, it has been shown previously that PTP-1B protein levels are up-regulated in cell lines derived from chronic myelogenous leukemia patients (19)(20)(21). These observations led us to investigate the role of PTP-1B in hematopoiesis and, in particular, myelopoie...

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Measurement ofCandida-specific blastogenesis: Comparison of carboxyfluorescein succinimidyl ester labelling of T cells, thymidine incorporation, and CD69 expression

Cited by 86 publications

References 0 publications

Leukocytosis, muscle damage and increased lymphocyte proliferative response after an adventure sprint race

Leukocytosis, muscle damage and increased lymphocyte proliferative response after an adventure sprint race

TC-PTP–deficient bone marrow stromal cells fail to support normal B lymphopoiesis due to abnormal secretion of interferon-γ

Protein tyrosine phosphatase 1B negatively regulates macrophage development through CSF-1 signaling

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