scholarly journals The role of the mitochondrial pore in the effector functions of human neutrophils

Immunologiya ◽  
2020 ◽  
Vol 41 (1) ◽  
pp. 42-53
Author(s):  
N.V. Vorobjeva ◽  
◽  
I.V. Kondratenko ◽  
S.S. Vakhlyarskaya ◽  
B.V. Chernyak ◽  
...  
Keyword(s):  
Human Neutrophils ◽  
Effector Functions ◽  
Mitochondrial Pore

The Signaling Pathways in Nitric Oxide Production by Neutrophils Exposed to N-nitrosodimethylamine

2018 ◽  
Vol 16 (2) ◽  
pp. 194-199
Author(s):  
Wioletta Ratajczak-Wrona ◽  
Ewa Jablonska
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Polymorphonuclear Neutrophils ◽  
Microbial Pathogens ◽  
Human Neutrophils ◽  
No Production ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Background: Polymorphonuclear neutrophils (PMNs) play a crucial role in the innate immune system’s response to microbial pathogens through the release of reactive nitrogen species, including Nitric Oxide (NO). </P><P> Methods: In neutrophils, NO is produced by the inducible Nitric Oxide Synthase (iNOS), which is regulated by various signaling pathways and transcription factors. N-nitrosodimethylamine (NDMA), a potential human carcinogen, affects immune cells. NDMA plays a major part in the growing incidence of cancers. Thanks to the increasing knowledge on the toxicological role of NDMA, the environmental factors that condition the exposure to this compound, especially its precursors- nitrates arouse wide concern. Results: In this article, we present a detailed summary of the molecular mechanisms of NDMA’s effect on the iNOS-dependent NO production in human neutrophils. Conclusion: This research contributes to a more complete understanding of the mechanisms that explain the changes that occur during nonspecific cellular responses to NDMA toxicity.

scholarly journals The Enigma of Eosinophil Degranulation

2021 ◽  
Vol 22 (13) ◽  
pp. 7091
Author(s):  
Timothée Fettrelet ◽  
Lea Gigon ◽  
Alexander Karaulov ◽  
Shida Yousefi ◽  
Hans-Uwe Simon
Keyword(s):  
Blood Cells ◽  
Inflammatory Diseases ◽  
White Blood Cells ◽  
Exact Role ◽  
Effector Cells ◽  
Effector Functions ◽  
Cytotoxic Effector ◽  
Eosinophil Degranulation

Eosinophils are specialized white blood cells, which are involved in the pathology of diverse allergic and nonallergic inflammatory diseases. Eosinophils are traditionally known as cytotoxic effector cells but have been suggested to additionally play a role in immunomodulation and maintenance of homeostasis. The exact role of these granule-containing leukocytes in health and diseases is still a matter of debate. Degranulation is one of the key effector functions of eosinophils in response to diverse stimuli. The different degranulation patterns occurring in eosinophils (piecemeal degranulation, exocytosis and cytolysis) have been extensively studied in the last few years. However, the exact mechanism of the diverse degranulation types remains unknown and is still under investigation. In this review, we focus on recent findings and highlight the diversity of stimulation and methods used to evaluate eosinophil degranulation.

scholarly journals Protein phosphatase inhibitors okadaic acid and calyculin A alter cell shape and F-actin distribution and inhibit stimulus-dependent increases in cytoskeletal actin of human neutrophils

Blood ◽  
1992 ◽  
Vol 80 (11) ◽  
pp. 2911-2919 ◽  
Author(s):  
P Kreienbuhl ◽  
H Keller ◽  
V Niggli
Keyword(s):  
Okadaic Acid ◽  
Human Neutrophils ◽  
Resting Cells ◽  
Calyculin A ◽  
Chemotactic Peptide ◽  
Phosphatase Inhibitors ◽  
Protein Phosphatase Inhibitors ◽  
Actin Localization ◽  
Shape Changes

Abstract The phosphatase inhibitors okadaic acid and calyculin A were found to elicit or to modify several neutrophil responses, suggesting that dephosphorylation plays a regulatory role. The concentrations of okadaic acid (> or = 1 mumol/L) that were effective on neutrophil functions (shape changes and marginal stimulation of pinocytosis) were shown to stimulate the incorporation of 32PO4 into many neutrophil proteins several-fold. Calyculin A was effective at 50-fold lower concentrations. In the presence of the inhibitors, the cells exhibited a nonpolar shape and the polarization response induced by chemotactic peptide was inhibited. Both phosphatase inhibitors also induced the association of F-actin with the cell membrane. A steady-state phosphatase activity is thus involved in maintaining shape and F-actin localization of resting cells. Inhibitors alone had no significant effect on the amount of cytoskeleton-associated actin. The increase in cytoskeletal actin observed at 30 minutes of stimulation with phorbol ester or 5 to 30 minutes of stimulation with chemotactic peptide, however, was abolished by okadaic acid or calyculin A, suggesting an important role of a phosphatase. In contrast, the early increase in cytoskeleton-associated actin observed at 1 minute of stimulation with peptide was not affected. This finding indicates that the increased association of actin with the cytoskeleton in the early and the later stages of neutrophil activation may be mediated by different signalling pathways.

scholarly journals Role of p38 MAPK in PMA‐induced NETs release from human neutrophils

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Ravi Shankar Keshari ◽  
Sachin Kumar ◽  
Anupam Jyoti ◽  
Satyananda Patel ◽  
Manoj Kumar Barthwal ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Human Neutrophils

The complex role of EZH2 in the tumor microenvironment: opportunities and challenges for immunotherapy combinations

2020 ◽  
Vol 12 (15) ◽  
pp. 1415-1430
Author(s):  
Jing Qiu ◽  
Shikhar Sharma ◽  
Robert A Rollins ◽  
Thomas A Paul
Keyword(s):  
Tumor Microenvironment ◽  
Cell Fate ◽  
Cell Function ◽  
Immune Dysfunction ◽  
Lymphoid Cells ◽  
Epigenetic Changes ◽  
Immune Effector ◽  
Effector Functions ◽  
Tumor Immunogenicity

Immune dysfunction in the tumor microenvironment occurs through epigenetic changes in both tumor cells and immune cells that alter transcriptional programs driving cell fate and cell function. Oncogenic activation of the histone methyltransferase EZH2 mediates gene expression changes, governing tumor immunogenicity as well as differentiation, survival and activation states of immune lineages. Emerging preclinical studies have highlighted the potential for EZH2 inhibitors to reverse epigenetic immune suppression in tumors and combine with immune checkpoint therapies. However, EZH2 activity is essential for the development of lymphoid cells, performing critical immune effector functions within tumors. In this review, we highlight the complexity of EZH2 function in immune regulation which may impact the implementation of combination with immunotherapy agents in clinic.

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