Autoantigen-specific immune tolerance in pathological and physiological cell death: Nanotechnology comes into view

2020 ◽  
pp. 107177
Author(s):  
Amir Tajbakhsh ◽  
Najmeh Farahani ◽  
Sayed Mohammad Gheibihayat ◽  
Amir Masoud Mirkhabbaz ◽  
Amir Savardashtaki ◽  
...  
Keyword(s):  
Cell Death ◽  
Immune Tolerance ◽  
Physiological Cell Death

Protein Synthesis during Programmed (Physiological) Cell Death

1991 ◽  
pp. 451-459
Author(s):  
R. A. Lockshin ◽  
Z. F. Zakeri ◽  
L. M. Yesner
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Physiological Cell Death

scholarly journals Cathepsin D gene expression outlines the areas of physiological cell death during embryonic development

2007 ◽  
Vol 236 (3) ◽  
pp. 880-885 ◽  
Author(s):  
V. Zuzarte-Luis ◽  
J.A. Montero ◽  
N. Torre-Perez ◽  
J.A. Garcia-Porrero ◽  
J.M. Hurle
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Embryonic Development ◽  
Cathepsin D ◽  
Physiological Cell Death

Cell-Adhesion to Crystal Surfaces: Adhesion-Induced Physiological Cell Death

1996 ◽  
Vol 4 (4-5) ◽  
pp. 341-353 ◽  
Author(s):  
Dorit Hanein ◽  
Anat Yarden ◽  
Helena Sabanay ◽  
Lia Addadi ◽  
Benjamin Geiger
Keyword(s):  
Cell Death ◽  
Cell Adhesion ◽  
Crystal Surfaces ◽  
Physiological Cell Death

The medical significance of physiological cell death

1995 ◽  
Vol 15 (4) ◽  
pp. 299-311 ◽  
Author(s):  
Georg Häucker ◽  
David L. Vaux
Keyword(s):  
Cell Death ◽  
Physiological Cell Death

The Role of the Pro-Apoptotic Bcl-2 Family Member Bim in Physiological Cell Death

2006 ◽  
Vol 926 (1) ◽  
pp. 83-89 ◽  
Author(s):  
PHILIPPE BOUILLET ◽  
DAVID C.S. HUANG ◽  
LORRAINE A. O'REILLY ◽  
HAMSA PUTHALAKATH ◽  
LIAM O'CONNOR ◽  
...  
Keyword(s):  
Cell Death ◽  
Family Member ◽  
Physiological Cell Death

scholarly journals Genome digestion is a dispensable consequence of physiological cell death mediated by cytotoxic T lymphocytes.

1992 ◽  
Vol 12 (7) ◽  
pp. 3060-3069 ◽  
Author(s):  
D S Ucker ◽  
P S Obermiller ◽  
W Eckhart ◽  
J R Apgar ◽  
N A Berger ◽  
...  
Keyword(s):  
Cell Death ◽  
Cytotoxic T Lymphocyte ◽  
Death Process ◽  
Cell Nuclei ◽  
Calcium Dependent ◽  
Nuclear Envelope Breakdown ◽  
Murine Fibroblast ◽  
Cell Death Process ◽  
Cell Suicide ◽  
Physiological Cell Death

We examined virally transformed murine fibroblast clones as targets for cytotoxic T lymphocyte (CTL)-triggered lysis and genome digestion. Strikingly, while all clones were essentially equivalent in the ability to be lysed, one clone, SV3T3-B2.1, failed to exhibit genome digestion associated with CTL attack. Other aspects of the physiological cell death process, including loss of adhesion and nuclear envelope breakdown (lamin phosphorylation and solubilization), were not altered in this clone. The absence of genome digestion associated with CTL-induced cell death correlated with the absence of endodeoxyribonuclease activity in the nuclei of that clone. Characterization of the activity affected identifies a calcium-dependent, DNase I-like endonuclease of approximately 40 kDa, normally present constitutively in all cell nuclei, as the enzyme responsible for genome digestion associated with CTL-mediated cell death. These observations indicate that neither genome digestion per se nor its consequences [such as activation of poly(ADP-ribose) polymerase] are essential for cell death resulting from the triggering of this cell suicide process.

scholarly journals PKHB1 Tumor Cell Lysate Induces Antitumor Immune System Stimulation and Tumor Regression in Syngeneic Mice with Tumoral T Lymphoblasts

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Ana Carolina Martínez-Torres ◽  
Kenny Misael Calvillo-Rodríguez ◽  
Ashanti Concepción Uscanga-Palomeque ◽  
Luis Gómez-Morales ◽  
Rodolfo Mendoza-Reveles ◽  
...  
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Tumor Cell ◽  
Immune Tolerance ◽  
Tumor Regression ◽  
Ex Vivo ◽  
Cell Lysate ◽  
Hematological Cancers ◽  
Tumor Cell Lysate

Acute lymphocytic leukemia (ALL) is the most common pediatric cancer. Currently, treatment options for patients with relapsed and refractory ALL mostly rely on immunotherapies. However, hematological cancers are commonly associated with a low immunogenicity and immune tolerance, which may contribute to leukemia relapse and the difficulties associated with the development of effective immunotherapies against this disease. We recently demonstrated that PKHB1, a TSP1-derived CD47 agonist peptide, induces immunogenic cell death (ICD) in T cell ALL (T-ALL). Cell death induced by PKHB1 on T-ALL cell lines and their homologous murine, L5178Y-R (T-murine tumor lymphoblast cell line), induced damage-associated molecular patterns (DAMPs) exposure and release. Additionally, a prophylactic vaccination with PKHB1-treated L5178Y-R cells prevented tumor establishment in vivo in all the cases. Due to the immunogenic potential of PKHB1-treated cells, in this study we assessed their ability to induce antitumor immune responses ex vivo and in vivo in an established tumor. We first confirmed the selectivity of cell death induced by PKBH1 in tumor L5178Y-R cells and observed that calreticulin exposure increased when cell death increased. Then, we found that the tumor cell lysate (TCL) obtained from PKHB1-treated L5178YR tumor cells (PKHB1-TCL) was able to induce, ex vivo, dendritic cells maturation, cytokine production, and T cell antitumor responses. Finally, our results show that in vivo, PKHB1-TCL treatment induces tumor regression in syngeneic mice transplanted with L5178Y-R cells, increasing their overall survival and protecting them from further tumor establishment after tumor rechallenge. Altogether our results highlight the immunogenicity of the cell death induced by PKHB1 activation of CD47 as a potential therapeutic tool to overcome the low immunogenicity and immune tolerance in T-ALL.

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