Internalization, lysosomal degradation and new synthesis of surface membrane CD4 in phorbol ester-activated T-lymphocytes and U-937 cells

1992 ◽  
Vol 201 (1) ◽  
pp. 160-173 ◽  
Author(s):  
C.Munck Petersen ◽  
E.Ilsø Christensen ◽  
B.Storstein Andresen ◽  
B.K. Møller
Keyword(s):  
T Lymphocytes ◽  
Phorbol Ester ◽  
Surface Membrane ◽  
Lysosomal Degradation ◽  
New Synthesis ◽  
Activated T Lymphocytes

scholarly journals BINDING OF AGGREGATED γ-GLOBULIN TO ACTIVATED T LYMPHOCYTES IN THE GUINEA PIG

1974 ◽  
Vol 139 (4) ◽  
pp. 1002-1012 ◽  
Author(s):  
John A. van Boxel ◽  
David L. Rosenstreich
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
T Lymphocytes ◽  
Guinea Pig ◽  
Surface Membrane ◽  
Cell Populations ◽  
Cell Marker ◽  
Activated T Cells ◽  
Activated T Lymphocytes

Heat-aggregated guinea pig γ-globulin was shown to bind to the surface membrane of a subclass of guinea pig T lymphocytes. Cells of this subpopulation were identified as T lymphocytes because these cells did not stain for surface Ig (a B-cell marker) but did form spontaneous E-rosettes with rabbit erythrocytes (a T-cell marker). A strikingly high proportion of such aggregate-binding (Agg+), E-rosette-forming (E-rosette+), but surface Ig-negative (Ig-) cells were found in an inflammatory exudate. Thus purified peritoneal exudate lymphocytes (PELs) are known to consist of over 90% T cells, and 59% of these cells bound aggregates. 10% of these Agg+ Ig- E-rosette+ cells were found in draining lymph node cell populations and none in thymus cell populations. The high frequency amongst PELs suggested that these Aggregate+ Ig- E-rosette+ cells might be activated T cells as these are known to occur in high proportion in PEL populations. Confirmatory evidence for this postulate was provided by the striking increase (from 10% to 46%) of Ig- E-rosette+ cells that bound aggregates when lymph node cells were activated by antigen stimulation in vitro.

scholarly journals Surface membrane CD4 turnover in phorbol ester stimulated T-lymphocytes

FEBS Letters ◽  
1990 ◽  
Vol 276 (1-2) ◽  
pp. 59-62 ◽  
Author(s):  
B.K. Møller ◽  
B.S. Andresen ◽  
E.Ilsø Christensen ◽  
C.Munck Petersen
Keyword(s):  
T Lymphocytes ◽  
Phorbol Ester ◽  
Surface Membrane

scholarly journals Characterization of β2 (CD18) integrin phosphorylation in phorbol ester-activated T lymphocytes

1999 ◽  
Vol 339 (1) ◽  
pp. 119 ◽  
Author(s):  
Leena VALMU ◽  
Tiina J. HILDEN ◽  
Gijsbert van WILLIGEN ◽  
Carl G. GAHMBERG
Keyword(s):  
T Lymphocytes ◽  
Phorbol Ester ◽  
Activated T Lymphocytes

scholarly journals The Emerging Roles of the Calcineurin-Nuclear Factor of Activated T-Lymphocytes Pathway in Nervous System Functions and Diseases

2016 ◽  
Vol 2016 ◽  
pp. 1-20 ◽  
Author(s):  
Maulilio John Kipanyula ◽  
Wahabu Hamisi Kimaro ◽  
Paul F. Seke Etet
Keyword(s):  
Nervous System ◽  
T Lymphocytes ◽  
Neurodegenerative Diseases ◽  
Psychotic Disorders ◽  
Spinal Cord Injuries ◽  
Metabolic Diseases ◽  
Nuclear Factor ◽  
Activated T Lymphocytes ◽  
Endogenous Regulators ◽  
Brain And Spinal Cord

The ongoing epidemics of metabolic diseases and increase in the older population have increased the incidences of neurodegenerative diseases. Evidence from murine and cell line models has implicated calcineurin-nuclear factor of activated T-lymphocytes (NFAT) signaling pathway, a Ca2+/calmodulin-dependent major proinflammatory pathway, in the pathogenesis of these diseases. Neurotoxins such as amyloid-β, tau protein, andα-synuclein trigger abnormal calcineurin/NFAT signaling activities. Additionally increased activities of endogenous regulators of calcineurin like plasma membrane Ca2+-ATPase (PMCA) and regulator of calcineurin 1 (RCAN1) also cause neuronal and glial loss and related functional alterations, in neurodegenerative diseases, psychotic disorders, epilepsy, and traumatic brain and spinal cord injuries. Treatment with calcineurin/NFAT inhibitors induces some degree of neuroprotection and decreased reactive gliosis in the central and peripheral nervous system. In this paper, we summarize and discuss the current understanding of the roles of calcineurin/NFAT signaling in physiology and pathologies of the adult and developing nervous system, with an emphasis on recent reports and cutting-edge findings. Calcineurin/NFAT signaling is known for its critical roles in the developing and adult nervous system. Its role in physiological and pathological processes is still controversial. However, available data suggest that its beneficial and detrimental effects are context-dependent. In view of recent reports calcineurin/NFAT signaling is likely to serve as a potential therapeutic target for neurodegenerative diseases and conditions. This review further highlights the need to characterize better all factors determining the outcome of calcineurin/NFAT signaling in diseases and the downstream targets mediating the beneficial and detrimental effects.

Proteinuria and Activated T-Lymphocytes in Diabetic Nephropathy

Diabetes ◽  
1988 ◽  
Vol 37 (5) ◽  
pp. 507-511 ◽  
Author(s):  
J. J. Bending ◽  
A. Lobo-Yeo ◽  
D. Vergani ◽  
G. Viberti
Keyword(s):  
Diabetic Nephropathy ◽  
T Lymphocytes ◽  
Activated T Lymphocytes

Specific features of T- and NK-cellular immunity in chronic lymphocytic leukemia

2021 ◽  
Vol 66 (6) ◽  
pp. 345-352
Author(s):  
Evgeniy Vladimirovich Pochtar ◽  
S. A. Lugovskaya ◽  
E. V. Naumova ◽  
E. A. Dmitrieva ◽  
A. I. Kostin ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Chronic Lymphocytic Leukemia ◽  
T Lymphocytes ◽  
Nk Cells ◽  
Lymphocytic Leukemia ◽  
Positive Trend ◽  
Functional Changes ◽  
Activated T Lymphocytes ◽  
T Helpers

Profound immunological dysfunction is the key factor determining the development of infectious complications in chronic lymphocytic leukemia (CLL). The aim of this work is to assess the features of the subpopulation composition of T-lymphocytes (T-helpers (Th), cytotoxic T-lymphocytes (Tcyt), T regulatory cells (Treg), T-NK cells, naive Th, Th-memory, activated T-lymphocytes, TCRγδ cells) and NK cells in peripheral blood of patients with newly diagnosed chronic lymphocytic leukemia (CLL) and receiving ibrutinib therapy. Hematological and immunophenotypic studies have been performed in 30 patients with previously untreated CLL, 122 patients on ibrutinib therapy and 20 healthy donors. The subpopulation composition of T-lymphocytes (Th, Tcyt, Treg, T-NK, naive T-helpers, memory T-helpers, TCRγδ cells, activated T-lymphocytes) and NK cells has been assessed on flow cytometer (FACSCanto II (BD)) using the following panel of monoclonal antibodies: CD45, CD19, CD3, CD4, CD5, CD8, TCRγδ, CD127, CD16, CD56, CD57 CD45RA, CD45R0, HLA-DR, CD25. Compared to controls all CLL samples were found to have higher the absolute number of T-lymphocytes, NK cells and their subpopulations, T-helpers (especially of memory T-cells), cytotoxic T-cells, regulatory T-cells, TCRγδ T-cells, activated T-lymphocytes, increased cytotoxic potential of NK cells in previously untreated CLL patients. Patients who received ibrutinib therapy have registered a positive trend towards recovery of the subpopulation composition of T-lymphocytes and NK-cells. CLL patients have been found to have quantitative and functional changes in the subpopulations of T-lymphocytes and NK cells, indicating dysregulation of the immune response, and a high risk of developing infections. Monitoring of immunological parameters for ibrutinib therapy make possible to estimate impact of ibrutinib on the adaptive anti-CLL immune response.

scholarly journals Doxorubicin activates nuclear factor of activated T-lymphocytes and Fas ligand transcription: role of mitochondrial reactive oxygen species and calcium

2005 ◽  
Vol 389 (2) ◽  
pp. 527-539 ◽  
Author(s):  
Shasi V. Kalivendi ◽  
Eugene A. Konorev ◽  
Sonya Cunningham ◽  
Sravan K. Vanamala ◽  
Eugene H. Kaji ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
T Lymphocytes ◽  
Fas Ligand ◽  
Reactive Oxygen ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Rat Cardiomyocytes ◽  
Activated T Lymphocytes ◽  
Pre Treatment ◽  
Fas L

Doxorubicin (DOX), a widely used antitumour drug, causes dose-dependent cardiotoxicity. Cardiac mitochondria represent a critical target organelle of toxicity during DOX chemotherapy. Proposed mechanisms include generation of ROS (reactive oxygen species) and disturbances in mitochondrial calcium homoeostasis. In the present study, we probed the mechanistic link between mitochondrial ROS and calcium in the embryonic rat heart-derived H9c2 cell line and in adult rat cardiomyocytes. The results show that DOX stimulates calcium/calcineurin-dependent activation of the transcription factor NFAT (nuclear factor of activated T-lymphocytes). Pre-treatment of cells with an intracellular calcium chelator abrogated DOX-induced nuclear NFAT translocation, Fas L (Fas ligand) expression and caspase activation, as did pre-treatment of cells with a mitochondria-targeted antioxidant, Mito-Q (a mitochondria-targeted antioxidant consisting of a mixture of mitoquinol and mitoquinone), or with adenoviral-over-expressed antioxidant enzymes. Treatment with GPx-1 (glutathione peroxidase 1), MnSOD (manganese superoxide dismutase) or a peptide inhibitor of NFAT also inhibited DOX-induced nuclear NFAT translocation. Pre-treatment of cells with a Fas L neutralizing antibody abrogated DOX-induced caspase-8- and -3-like activities during the initial stages of apoptosis. We conclude that mitochondria-derived ROS and calcium play a key role in stimulating DOX-induced ‘intrinsic and extrinsic forms’ of apoptosis in cardiac cells with Fas L expression via the NFAT signalling mechanism. Implications of ROS- and calcium-dependent NFAT signalling in DOX-induced apoptosis are discussed.

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