Modulation of T Cell Morphology and Induction of Homotypic Adhesion by a Protein Tyrosine Kinase Inhibitor

Butler, Yun X.; Tibbetts, Scott A.; Chirathaworn, Chintana; Benedict, Stephen H.

doi:10.1006/cimm.1995.1107

Cited by 8 publications

(2 citation statements)

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“…Protein tyrosine kinase inhibitors have been shown to inhibit induction of the morphological alterations associated with adhesion. 29 Genistein has been reported to partially inhibit SCF‐induced adhesion of mast cells. 13 It has been shown that c ‐ kit exhibits intrinsic tyrosine kinase activity, and tyrosine kinase activity is postulated to play a role in signalling through this receptor.…”

Section: Resultsmentioning

confidence: 99%

Morphological alterations in rat peritoneal mast cells by stem cell factor

1998

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SUMMARYStem cell factor (SCF ) stimulates mast cell adhesion and, because SCF is produced normally in tissues, it may be a major factor responsible for the adhesion of mast cells to connective tissue matrix. We found that the morphology of rat peritoneal mast cells (RPMC ) altered after the addition of recombinant murine SCF (rmSCF ) in vitro. The ability of rmSCF to enhance morphological alteration was dose dependent and completely abolished by anti-c-kit ACK2 monoclonal antibody. Exposure of RPMC to transforming growth factor-b 1 , wortmannin, genistein, herbimycin A, staurosporine, indomethacin and cytochalasin D before the addition of rmSCF antagonized rmSCF-induced morphological alteration. However, nordihydroguiaretic acid had no effect. Many RPMC appeared to respond also to nerve growth factor (NGF ) but the total number of cells with altered morphology was much greater when the culture was stimulated by rmSCF than by NGF. We suggest that morphological alterations of mast cells by rmSCF is an important step for the participation in adhesion to tissue under resident physiological conditions.

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Section: Resultsmentioning

confidence: 99%

Morphological alterations in rat peritoneal mast cells by stem cell factor

1998

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“…Cells were incubated at 37 °C inmidified CO 2 incubator for 72 hours. Proliferation was assessed using an MTT assay (Mit-T-kit, BCD Labs, Lawrence, KS) as previously described (1). The MTT assay measured the ability of cell mitochondria to convert MTT [(3-(4,5-dimethylthiazol-2-yl)-2,5,-diphenyl tetrazolium bromide] to a blue formazan product (13).…”

Section: Lymphocyte Proliferation Assaymentioning

confidence: 99%

Minimal Influence of Carbohydrate Ingestion on the Immune Response Following Acute Resistance Exercise

Koch¹,

Potteiger²,

Chan³

et al. 2001

International Journal of Sport Nutrition and Exercise Metabolism

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The effect of carbohydrate supplementation (CHO) on the lymphocyte response to acute resistance exercise was examined in 10 resistance-trained males. Subjects completed a randomized double-blind protocol with sessions separated by 14 days. The exercise session consisted of a high intensity, short rest interval squat workout. Subjects consumed 1.0 g á kg body mass(-1) CHO or an equal volume of placebo (PLC) 10 min prior to and 10 min following exercise. Blood was collected at rest (REST), immediately post exercise (POST), and at 1.5 hours and 4.0 hours of recovery, and analyzed for plasma glucose, serum cortisol, leukocyte subsets, and phytohemagglutinin (PHA)-stimulated lymphocyte proliferation. A significant Treatment 3 Time effect was observed for lymphocyte proliferation between CHO and PLC, but post hoc analyses revealed no between-treatment differences at any post-exercise time point. Lymphocyte proliferation was significantly depressed below REST at POST (-39.2% for PLC, -25.7% for CHO). Significant fluctuations in leukocyte subset trafficking were observed for both treatments at POST, 1.5 hours, and 4.0 hours. Plasma glucose was significantly increased POST in CHO compared to PLC. Cortisol was significantly increased from REST to POST in both treatments. These data support a minimal effect of carbohydrate ingestion on the lymphocyte response to high-intensity resistance exercise.

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The Adhesion of Anti-CD3-Activated Mouse T Cells to Syngeneic Colon Adenocarcinoma Cells Is Differentially Regulated by Protein Tyrosine Kinase-, Protein Kinase C-, and cAMP-Dependent Pathways in the Effector Cell

MacKenzie

Blay

1999

Biochemical and Biophysical Research Communications

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Modulation of T Cell Morphology and Induction of Homotypic Adhesion by a Protein Tyrosine Kinase Inhibitor

Cited by 8 publications

References 0 publications

Morphological alterations in rat peritoneal mast cells by stem cell factor

Morphological alterations in rat peritoneal mast cells by stem cell factor

Minimal Influence of Carbohydrate Ingestion on the Immune Response Following Acute Resistance Exercise

The Adhesion of Anti-CD3-Activated Mouse T Cells to Syngeneic Colon Adenocarcinoma Cells Is Differentially Regulated by Protein Tyrosine Kinase-, Protein Kinase C-, and cAMP-Dependent Pathways in the Effector Cell

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