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Anti-Arthritic Potential of Gold Nanoparticle
Published in Klaus D. Sattler, st Century Nanoscience – A Handbook, 2020
Jayeeta Sengupta, Sourav Ghosh, Antony Gomes
When T lymphocyte interacts with MHC on antigen-presenting cells, it may be activated, or show tolerance to the antigen, or undergo programmed cell death, depending on a second signal through appointing additional cellular receptors. The CD24 molecule on the T-cell surface may act as this second signal of costimulation. Activated T cells proliferate and secrete additional cytokines such as interleukin-2, interleukin-4, tumor necrosis factor, and interferon-γ. Interleukin-2 amplifies the proliferation of T cells. Very early inflamed synovium has been found to have an unexpected T helper cell profile, along with increased expression of interleukin-4, interleukin-5, and interleukin-13. When the diseased is established, synovial T cells produce low amounts of interferon-γ, interleukin-10, and tumor necrosis factor-α, while interleukin-2 and interleukin-4 become virtually absent. Interleukin-17 is produced spontaneously in synovial cells of rheumatoid arthritis patients. Interleukin-23 promotes the survival and proliferation of T helper cells. The receptor for interleukin-17 is expressed all over the synovium and exerts pleiotropic effects. Thus, T-cell-derived interleukin-17 (subtypes 17A and 17F) promotes monocyte-dependent interleukin-1 and tumor necrosis factor-α production and induces osteoclast differentiating factor RANKL (receptor activator of nuclear factor kappa-B ligand), stimulating synovial fibroblasts to express interleukin-6, interleukin-8, granulocyte colony-stimulating factor, prostaglandin E2, and matrix metalloproteinases.
Preformulation of New Biological Entities
Published in Sandeep Nema, John D. Ludwig, Parenteral Medications, 2019
Riccardo Torosantucci, Vasco Filipe, Jonathan Kingsbury, Atul Saluja, Yatin Gokarn
Cytokines are small hormone proteins that act in cell signaling pathways, most commonly in the activation of immune system components such as lymphocytes and macrophages. Interferons are potent glycoprotein cytokines with antiviral properties and can suppress uncontrolled cell proliferation. They have been used in the treatment of multiple sclerosis, immunological cancers, and hepatitis. Biotherapeutic interferons include interferon-α (e.g., Roferon-A®, Intron-A®, and Alferon-N®), interferon-β (e.g., Avonex®, Betaseron®, and Extavia®), and interferon-γ (e.g., Actimmune®). Similar to the interferons, the interleukins function as biochemical signals during immune response, with either stimulatory or inhibitory activities. For example, interleukin-1 (IL-1) controls pro-inflammatory reactions in response to tissue injury by pathogen- or danger-associated molecular patterns. Therefore, IL-1 receptor antagonists, such as anakinra (Kineret®), can be used in the treatment of inflammatory conditions such as rheumatoid arthritis. Recombinant interleukin-2 (IL-2), aldesleukin (Proleukin®), stimulates T cells and is used in the treatment of metastatic renal cell carcinoma and melanoma.
Mechanistic Model of Tumor Response to Immunotherapy
Published in Vittorio Cristini, Eugene J. Koay, Zhihui Wang, An Introduction to Physical Oncology, 2017
Geoffrey V. Martin, Eman Simbawa
The role of the immune system in fighting cancer and how immune system inhibition can promote tumor growth has been an area of active research over the past few decades. This relationship between the immune system and the tumor microenvironment is complex, however, as different immune cells can have tumor-suppressive and tumor-promoting properties [324,325]. Furthermore, the interaction between immune cells and cancer cells is likely dependent on a multitude of factors, including tumor antigenicity, individual genetic heterogeneity, prior antigen exposure, tumor vasculature, and nonimmune tumor stromal content [324]. Despite these complexities, the immune system has been shown to have prognostic ramifications in multiple cancer types, with studies demonstrating an association between increased immune cell tumor infiltration on pathologic specimens of colon, endometrial, esophageal, and ovarian cancers and improved disease outcomes [326–329]. Understanding the exact mechanisms of immune system suppression of cancer has led to the development of immune-modulating cancer treatments (immunotherapy), including interleukin-2 (IL-2), vaccine-based therapies, and immune checkpoint inhibitors, with promising results in recent clinical trials [330–335]. In this chapter, we explore general strategies for mathematical modeling of immune system and tumor interaction, as well as specific examples of immunotherapy modeling, which focuses on the application of these computational models in clinical scenarios.
Intelligent solution predictive networks for non-linear tumor-immune delayed model
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Nabeela Anwar, Iftikhar Ahmad, Adiqa Kausar Kiani, Muhammad Shoaib, Muhammad Asif Zahoor Raja
The immunologic helps in the fighting against cancer cells as the body’s natural defensive system. Nowadays, one of the most essential aspects of cancer cellular biology is how the body’s immune system reacts to the progression of cancer (de Pillis et al. 2006). Despite medical advancements, there are still significant problems in the diagnosis and treatments of cancer disease that have prevailed for the past 20 years. Our immune system is made up of several types of lymphoid tissues, cytokines and cells that protect our bodies from various infections and foreign pathogens, particularly cancer cells. Immune effector cells include B-lymphocytes, T-lymphocytes, macrophages and natural killer cells (Eskandari et al. 2022). When the body’s immune system detects cancer cells, our immune system reacts. The immune system usually identified the cancer cells but the response of the immune system may be inefficient and unable to target tumor cells. The existence of cancer cells stimulates the development of effective cells. Cancer cells as well as effective cells are the primary predators in our bodies. Interleukin-2 is a cytokine produced by CD4 + T lymphocytes that encourages immune cell proliferation to defeat more malignant cells (Eskandari et al. 2022; Saifullah et al. 2022).