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Studies on NK Cell Precursors in Mice
Published in Ronald H. Goldfarb, Theresa L. Whiteside, Tumor Immunology and Cancer Therapy, 2020
Carlo Riccardi, Emira Ayroldi, Lorenza Cannarile, Domenico Delfino, Francesca D’Adamio, Luciano D’Adamio, Graziella Migliorati
Using this system we have shown that in vivo treatment with CKs, including IL-2 and interferons (IFNs), soon after BM graft or in vitro pretreatment of donor BM cells before transplant, results in a significant increase of NK cell activity reconstitution (13,17). These data suggest that IL-2 and IFNs can influence the development of NK cell precursors participating in the in vivo reconstitution of reactivity. Similar results have also been obtained with IL-1, TNFα and LT (2). Combination of two or more CKs induces a synergic effect and the increased reconstitution of NK activity correlates well with increased tumor resistance (2).
Outdoor Air Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
The mRNA that encodes the CKs are unstable. Consequently, the secretion of CKs is brief and self-limiting, so the intervention of more CKs “in relay” is necessary to support a biologically targeted effect (teleonomy of the natural phenomena). The clinician dealing with severe chemical sensitivity will see this phenomenon in that until the total body pollutant load is decreased, intradermal neutralization treatment cannot be accomplished because the specific treatment endpoints constantly change due to the unstable CKs. When the injections are administered, they reproduce patient's symptoms but then a proper dilution eliminates symptoms; the clinician can then give a treatment dilution that can be efficacious turning off the clinical reaction. Once the RNA is stabilized, the individual patient can then take treatment and do well. Thus, it only occurs with the combination of elimination of the triggering agents and the proper injection neutralizing dose. This is the importance for decreasing the total body pollutant load which is the most important modality to succeed by avoidance of pollutants in air, food, and water.
Basic Knowledge of Host Defenses Against Infection
Published in M. T. Labro, Host Defense and Infection, 1994
The term cytokines (CK) covers a wide and still growing number or molecules endowed with cell regulatory properties, also called lymphokines or monokines (depending on their origin), interleukins, interferons and cell-stimulating factors (CSFs). They represent an “intercellular language” and play significant roles in growth, differentiation, host defenses and tissue damages. From the first interleukin (IL-1) discovered in 1972 till the last one, IL- 13 (1993), much has been learned about the structure, properties and functions of these factors; the cloning of the CK genes and of most CK receptors, as well as their widespread availability, has led to an explosion of scientific knowledge. CKs, although a heterogeneous group of proteins, have some common characteristics: low molecular weight (<80 kD), glycosylation, transient and local production, effects mediated in a paracrine or autocrine (rather than endocrine) manner, interaction with high-affinity cell surface receptors expressed at a relatively low number (10-10000/cell) and extreme potency (acting at picomolar concentrations). CKs have multiple, overlapping cell regulatory actions. For instance, IL-1, IL-6 and TNF mediate common effects. CKs form a complex network and may induce one another, transmodulate receptors or display synergistic, additive or antagonistic effects on cell functions. This network is under complex control at the transcriptional, translational and post translational level. The presence of endogenous CK receptor antagonists (IL-1-Ra, TNF inhibitors, etc.) may provide yet another means of influencing the final response to some CK. At the present time, it is almost impossible to draw a clear picture of CK sequential modulatory pathways in the infectious disease state, since pathogens interfere with various host defense components and different effectors are involved depending on the pathogen.
Chromosomal 1q21 abnormalities in multiple myeloma: a review of translational, clinical research, and therapeutic strategies
Published in Expert Review of Hematology, 2021
Kamlesh Bisht, Brian Walker, Shaji K. Kumar, Ivan Spicka, Philippe Moreau, Tom Martin, Luciano J. Costa, Joshua Richter, Taro Fukao, Sandrine Macé, Helgi van de Velde
Copy number gain of 1q21 is among the most common chromosomal aberrations in MM, observed in approximately 28−44% of patients at diagnosis [4–9]. It manifests in a tumor subclone as a secondary genomic event, becoming more frequent, and amplified as the tumor progresses [10]. In MM cells harboring 1q21+, oncogenesis and drug resistance are driven, at least in part, by upregulation of genes located in the 1q21 amplicon. Several genes on chromosome 1q are strongly associated with aggressive MM cell phenotypes, including CKS1B, PSMD4, ANP32E, and MCL-1. 1q21+ is divided into either 1q21 gain (3 copies) or 1q21 amplification (≥4 copies), with worse prognosis for patients with amplification than those with gain, though this finding has not been universal [8,10,11]. Co-existence of other chromosomal abnormalities such as t(4;14), t(14;16), del(1p), and del(17p) are common and further worsen the prognosis for patients with 1q21+ [10].
A review on proteomics analysis to reveal biological pathways and predictive proteins in sulfur mustard exposed patients: roles of inflammation and oxidative stress
Published in Inhalation Toxicology, 2019
Hojat Borna, Seyed Hojjat Hosseini Qale Noe, Asghar Beigi Harchegani, Nima Rahmani Talatappe, Mahdi Ghatrehsamani, Mostafa Ghanei, Alireza Shahriary
Keratins are the intermediate filaments-forming proteins which protect epithelial cell integrity against mechanical and non-mechanical stress (Coulombe & Omary, 2002). Previous studies showed the relationship between cytokeratins (CKs) expression and the regenerative or pathological status of the tracheobronchial epithelium in the lung (Iyonaga et al., 1997). Overexpression of CKs was found in lung biopsies of patients with idiopathic pulmonary fibrosis (Iyonaga et al., 1997). CKs are also highly expressed in different cancer types (Karantza, 2011). The effect of SM on keratin proteins within keratinocytes has also been studied. A proteomic based study on serum of SM exposed patients with chronic lung injury showed higher expression of CKs-1, -9 and -10 (Pashandi et al., 2015) (Table 1). In a proteome analysis study, increased breakdown of K14, K16 and K17 was observed in SM-exposed human keratinocyte cells at acute phase (Mol et al., 2008) (Table 1). Hess & FitzGerald (2007) revealed that SM can result in keratin filament destruction, leading to lysis of epidermal basal cells and skin blistering. Therefore, keratin overexpression may be a reason for altering tissues organization and injuries in SM exposed patients.
Maintaining therapeutic progress in multiple myeloma by integrating genetic and biological advances into the clinic
Published in Expert Review of Hematology, 2018
Gain of chromosome1q+ is seen in 40% of cases at diagnosis and is a key prognostic factor with the number of copies being critical. Beneath this level, amp1q, defined as >4 copies is present in 10% of NDMM and is tightly linked to adverse prognosis and HR disease. Amp1q arises via a number of different mechanisms including the formation of derivatives with multiple copy number gains by multiple cycles of break-fusion-bridge leading to the amplification of a transcriptional unit at 1q21 comprising a number of key genes including CKS1B, MCL1, and ANP32E. The gene responsible for HR disease is unknown and possibly the deregulation of the whole unit which contains many interesting genes, is important. Investigation in solid tumors has suggested that amp1q may be due to hypoxia and the expression of KDM4A [72]. The other mechanisms leading to amp1q are invisible to molecular approaches, including multiple translocations of 1q, whole arm translocations mediated by jumping 1q events mediated by the unstable pericentromeric chromatin on 1q, and the formation of isochromes of chromosome 1q where the p arm is lost simultaneously which is among the most adverse prognostic groups.