Effector Mechanisms for Macrophage-Induced Cytostasis and Cytolysis of Tumor Cells
Gloria H. Heppner, Amy M. Fulton in Macrophages and Cancer, 2019
In the previous section we discussed the kinetics of cytolysis. Prior to cell death, however, activated macrophages induce tumor cell cytostasis. In addition, some tumor cell phenotypes may not progress to cytolysis after developing cytostasis.36 A major question, which has eluded an answer, is whether cytostasis is concomitant with, independent of, or a prerequisite for cell death. Current dogma also holds that macrophages kill neoplastic and transformed cells but spare normal cells. In a review of the literature, we were unable to find any reports on whether macrophages caused cytostasis in normal cells. Accordingly, we designed experiments to determine if macrophages inhibit the progression through the cell cycle of normal fibroblasts even though they do not kill them.49
Histocompatibility Typing by Polyclonal and Cloned Human Cytotoxic T Lymphocytes
Soldano Ferrone, B. G. Solheim in HLA Typing: Methodology and Clinical Aspects, 2019
The following general rules are accepted in specificity studies on the effector phase of unrestricted, allogeneic CTL: Within the responding population of PBL, clones are not activated by antigenic determinants possessed by the individual from which they originate (self-tolerance).Within the responding populations of PBL, clones may, in principle, be activated against any determinant present in the stimulating/immunizing population of cells.Cytolysis is obtained from target cells possessing one or more of the antigenic determinants presented by the stimulating/immunizing population of cells.Conversely, if cytolysis is obtained with a given target cell, this would imply sharing of antigenic determinants between target and stimulating cells or eventual presentation of a cross-reactive determinant(s).
Dermal filler complications and management
Michael Parker, Charlie James in Fundamentals for Cosmetic Practice, 2022
The complement system is comprised of approximately thirty proteins which are synthesised by the liver and are permanently in circulation in blood plasma. When complement proteins are triggered by microbial antigens, a cascade of events is initiated with the intention of destroying pathogens through phagocytosis, cytolysis and inflammation. Phagocytosis is triggered via a process called opsonisation, where opsonin proteins are used to mark infected or dying cells to be phagocytosed. Cytolysis occurs through the formation of the membrane attack complex (MAC) which effectively punches a hole within the plasma membrane of bacteria, causing them to rupture due to an inflow of extracellular fluid. Finally, inflammation is stimulated by the binding of complement proteins to mast cells to encourage them to secrete histamine which increases blood vessel permeability to allow cells of the immune system to extravasate and reach the target area.
Synergistic Therapeutic Effects of Probiotic Lactobacillus casei TD-2 Consumption on GM-CSF-Induced Immune Responses in a Murine Model of Cervical Cancer
Published in Nutrition and Cancer, 2022
Elahe Abdolalipour, Mehran Mahooti, Ali Gorji, Amir Ghaemi
Spleens of three mice per group were removed seven days after the last treatment and then a single-cell suspension of splenocytes was provided from each spleen which were used as effector cells. 20000 EL4 cells in a volume of 100 µl (as a target cells) were cultured with the effector cells (splenocytes cells) (100 µl) at 50:1 rate for 8 h in phenol-red-free RPMI 1640 containing 3% FBS. For the preparation of target cells, following EL4 cells stimulation with a synthetic E7-specific CTL epitope at a concentration of 1 mg/ml, incubation for four hours was performed. After centrifugation, the co-culture supernatants (50 µl/well) were transferred to 96-well flat-bottom plates, and lysis of target cells was determined by assaying lactate dehydrogenase (LDH) release using an LDH Cytotoxicity Detection Kit (Takara BIO INC, Shiga, Japan) according to the instructions provided by the manufacturer. For all samples, including the controls, the assay was conducted in triplicate. The LDH-mediated conversion of a tetrazolium salt into a red formazan product was estimated at 490 nm after incubation at room temperature for 30 min. The spontaneous LDH release by target cells or effector cells was measured by incubation of target cells in the absence of effector cells and vice versa. The highest release of LDH was determined by incubation of the target cells in 1% Triton X-100 in an assay medium. The percentage of specific cytolysis was determined by the following formula:
Methotrexate enhances oxidative stress, apoptosis, and ultrastructural alterations in the placenta of rat
Published in Ultrastructural Pathology, 2022
Amany Mohamed Shalaby, Khalid Mohammed Mohammed Albakoush, Mohamed Ali Alabiad, Mohammed Alorini, Fatima A. Jaber, Mahmoud Ramadan Elkholy, Shereen Elsayed Tawfeek
Cystic degeneration of glycogen cells in the MTX-exposed placenta detected in our study was distinguished by aberrant preservation of large amounts of cytoplasmic vacuolation of glycogen cells. Eosinophilic fibrinous material was found in these vacuoles. The degraded cells underwent cytolysis and then coalesced into a series of giant cysts filled with a homogenous acidophilic mass, many leftover glycogen clusters, erythrocytes, macrophages, and cell debris. These degraded cells did not regress. Although in normal development, the majority of glycogen cells vanish at the completion of pregnancy.2 In animal studies, many substances cause the cystic degeneration of glycogen cells, such as 6-mercaptopurine14 and streptozotocin.21
Silk peptide treatment potentiates natural killer cell activity in vitro and induces natural killer cell maturation and activation in mouse splenocytes
Published in Pharmaceutical Biology, 2019
Sun-Hee Jang, Mi-Sun Oh, Hyang-Im Baek, Ki-Chan Ha, Jeong-Yong Lee, Yong-Suk Jang
Cytolytic activity in the immune system is essential for maintaining health, as it ensures the removal of pathogen-infected and malignantly transformed cells. NK cells are specialized cytotoxic innate immune cells that directly kill both virus-infected and abnormal cells (Topham and Hewitt 2009). In this context, we previously explored the effects of silk peptide on immune capability in vivo (Jang et al. 2018), specifically by promoting NK cell activity in mice. In this study, we investigated whether silk peptide modulates NK cells using NK cell line and ex vivo splenocytes. We observed increased NK-92MI NK cell activity (Figure 2) and increased expression of cell surface CD107a and intracellular IFN-γ (Figure 3) following treatment with silk peptide in vitro. Silk peptide-mediated enhancement of cytolytic activity against YAC-1 cells (Figure 4) and NK cell maturation (Figure 6) were also observed ex vivo in splenocytes. NK cells do not have antigen-specific receptors, instead expressing various germ-line encoded immune receptors that modulate NK cell activity. The ability of NK cells to recognize target cells is mediated by signaling based on the activation of NKG2D, Ly49D, DNAM-1, and natural cytotoxicity receptors. The fine balance and integration of signals from activating and inhibitory receptors regulates cytolytic activity in NK cells (Watzl and Long 2010). Importantly, we found that silk peptide treatment of ex vivo splenocytes increased the expression of NK cell activation markers including NKG2D, Nkp46, KLRG1 and Ly49D (Figure 7). These results suggest that silk peptide can induce NK cell activation signals that promote enhanced NK cell maturation and cytolytic activity.
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