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Immunomodulatory Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Cytokines differ from hormones, which are also important cell signaling molecules, in that hormones circulate in much lower concentrations and are made by specific kinds of cells (e.g., insulin from the beta cells of the pancreas). Whereas hormones circulate in nanomolar (10−9 M) concentrations that usually vary by less than a 10-fold order of magnitude, in contrast some cytokines such as IL-6 circulate in picomolar (10−12 M) concentrations that can increase by up to a 1,000-fold during trauma or infection.
Inflammation and immunology
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Christopher Bellamy, Stephen J. Jenkins, Henry J. McSorley, David A. Dorward, Timothy J. Kendall
These are rare, often life-threatening diseases that nevertheless have contributed greatly to our understanding of the immune system. X-linked agammaglobulinaemia is the most common of these disorders and is caused by a failure of cell signalling and maturation of B cells, with failure of the light chain gene rearrangement which normally allows the formation of Ig molecules. Circulating B cells are markedly reduced or absent and there is a failure to make antibody. Once maternal antibody has declined the children become susceptible to recurrent episodes of bacterial infection.
Disease Prediction and Drug Development
Published in Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam, Introduction to Computational Health Informatics, 2019
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam
The human-body has many types of cell signaling pathways such as: 1) cell-growth; 2) programmed cell-death; 3) cytoskeleton and extracellular matrix; 4) disease drivers, EMT (Epithelial-Mesenchymal Transition for wound healing) and angiogenesis (generation of blood-vessels); 5) epigenetics (changes in the organism due to gene-expression variations); 6) immune cell signaling and 7) neurodegenerative signaling.
Advancements in ocular gene therapy delivery: vectors and subretinal, intravitreal, and suprachoroidal techniques
Published in Expert Opinion on Biological Therapy, 2022
Kyle D Kovacs, Thomas A Ciulla, Szilárd Kiss
There is also extensive preclinical work being conducted on gene-independent but pathway-specific gene therapy for IRDs. Gene therapy can be used to target downstream effects on the cell signaling cascade induced by the primary underlying genetic mutation. While obviously not correcting the underlying IRD-driving genetic defect, modulating the downstream effects allows for a degree of neuroprotection and prolongation of cell survival. For example, targeting the mammalian target of rapamycin (mTOR) pathway has been previously shown to hold neuroprotection for photoreceptors, and subsequent work with AAV-mediated gene augmentation in a murine model of RP also demonstrated a protective effect [57,58]. Similar concepts have been employed with oxidative stress reduction by looking at Nrf2 manipulation, among others, in altering photoreceptor nutrient processing or decreasing endoplasmic reticulum stress [59–61]. These represent but a few of the efforts that have been undertaken to increase cell function and survival in the diseased state. The strategies hold great translational potential for prolonging cell survival in a more universal manner by allowing for gene-independent approaches to a range of IRDs.
Targeted therapy of tumour microenvironment by gold nanoparticles as a new therapeutic approach
Published in Journal of Drug Targeting, 2022
Negah Mahhengam, Kimia Kazemnezhad, Hendrik Setia Budi, Mohammad Javed Ansari, Dmitry Olegovich Bokov, Wanich Suksatan, Lakshmi Thangavelu, Homayoon Siahmansouri
Cytokines are small proteins that have a significant role in cell signalling and act as an immunomodulator through paracrine and autocrine mechanisms. Stromal and immune cells, like endothelial and fibroblasts cells, release them and control proliferation, differentiation, cell survival, activation of immune cells, migration, as well as death. In the TME, cytokines can adjust an anti-tumour response. Whereas, within chronic inflammation, these small molecules can induce transformation of cells and malignancy. This phenomenon is seen under certain conditions, such as the equivalence of pro-inflammatory/anti-inflammatory cytokines, their concentrations, the profile of cytokine receptor expression, and the activation pattern of nearby cells [153]. Cytokines that exist in the TME are summarised in table 1.
Primary Immunodeficiency and Thrombocytopenia
Published in International Reviews of Immunology, 2022
Maryam Mohtashami, Azadehsadat Razavi, Hassan Abolhassani, Asghar Aghamohammadi, Reza Yazdani
Some immune deficiencies are closely related to decrease platelet generation in this category. For example, FOXP3 gene disruption in T- cell signaling pathway causes immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome, which affects T- cells regulatory function [267]. This gene has important roles in immune regulation. It has been demonstrated that PRKCD and IPEX deficiency not only decrease platelet activation, but also reduces platelet production derived from megakaryocytes, which ultimately lead to thrombocytopenia [268–272]. Additionally, the ALPS-FASLG signaling pathway, as the first one deficiency, describes a condition that autoimmune lymph proliferative syndrome (ALPS) result from FASLG deficiency [273]. The majority effect of FAS-associated death domain (FADD) deficiency on T and B cells is stimulated by apoptosis via FAS molecule. Furthermore, FADD is accompanied by proliferative responses in B cells via TLR3- and TLR4 [274]. On the other hand, the interaction between Caspases 8, 10 and FAS-associated protein with the death domain of FAS has an essential function in platelet production. Despite regulating the apoptosis pathway, previous studies have demonstrated that FAS and FAS-associated proteins with the death domain are capable to induce necrosis when caspases inhibit. Thus, in ALPS and FADD deficiency, caspase-8 and caspase 10 absence or reduction of caspases can lead to necrosis in megakaryocytes, consequently, platelet count decreased [275–277].