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Porous Carbon Nanostructured Sorbents for Biomedical Application
Published in Zulkhair A. Mansurov, Carbon Nanomaterials in Biomedicine and the Environment, 2020
Almagul R. Kerimkulova, Seitkhan Azat, Zulkhair A. Mansurov
Interleukin-2 plays an important role in the initiation process and the development of immune response and has multiple effects on various components and links of the immune system [43]. The biological effects of interleukin-2 are mediated by its binding with specific receptors and presented on various cellular targets. The synthesized interleukin-2 works on T-lymphocytes, enhancing their proliferation and subsequent synthesis of interleukin-2. Interleukin-2 directly results in the growth, differentiation, and activation of T- and B-lymphocytes, mid cells, macrophages, oligodendroglioma cells, Langerhans cells. Interleukin-2 causes the formation of lymphokine-activated killers and activated the tumor cells [40]. The spectrum broadening of lysis effect of effector cells causes the destruction of various pathogenic microorganisms and infected cells, which provides immune protection directed against tumor cells, as well as pathogens of viral, bacterial and fungal infections. The creation of new sorbent is very important for the development of production effective method of interleukin-2, which can be successfully used to treat severe diseases such as bronchial asthma, peptic ulcer, tuberculosis, hepatitis C, brucellosis, osteomyelitis, tick-borne encephalitis, meningitis and herpetic infection.
Anti-Arthritic Potential of Gold Nanoparticle
Published in Klaus D. Sattler, st Century Nanoscience – A Handbook, 2020
Jayeeta Sengupta, Sourav Ghosh, Antony Gomes
Effector cells mediate maximum damage in rheumatoid arthritis, through the production of cytokines and other mediators. Macrophages act as the mastermind in the pathogenesis of the disease, producing pro-inflammatory cytokines including interleukin-1, interleukin-6, interleukin-8, tumor necrosis factor, and granulocyte-macrophage colony-stimulating factor, which further stimulates the macrophages and amplifies local and systemic inflammation, leading to synovial matrix destruction. These cytokines also activate other cells in the synovium (including osteoclast and fibroblasts) and cells in the liver (for production of C-reactive protein), contributing to the pathogenesis of rheumatoid arthritis. Activated macrophages also produce leukotrienes, prostaglandins, NO, and many other pro-inflammatory substances causing systemic and local inflammation. Local actions of macrophages include recruitment and potentiation of inflammatory cells, production of matrix-degrading proteolytic enzymes, and cytokine-induced differentiation of synovial cells and angiogenesis, whereas macrophage systemically intensifies rheumatoid arthritis, produces tumor necrosis factor, and activates circulating monocytes. Fibroblasts in the synovium secrete interleukin-6, interleukin-8, granulocyte-macrophage colony-stimulating factor, proteases, and collagenase, contributing to the pathogenesis of the disease. Neutrophils are the most abundant cell types found in the synovium of rheumatoid arthritis. Interleukin-8, leukotriene, and activation of complement pathway recruit neutrophils in the synovium, causing the generation of reactive oxygen species that depolymerize hyaluronic acid. Reactive oxygen species also inactivates protease inhibitors, causing protein denaturation at the synovium. Interleukin-1 and tumor necrosis factor activate chondrocytes to produce a significant amount of proteases causing the destruction of cartilage matrix.
An immune cell infiltration landscape classification to predict prognosis and immunotherapy effect in oral squamous cell carcinoma
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Tumor immunotherapy includes stimulating the immune system, proliferating and stimulating effector cells to infiltrate the tumor microenvironment (TME), and destroying tumor cells (Arneth 2019). For the past few years, the significance of tumor-infiltrating lymphocytes (TILs) in treating various tumors has become a research hotspot. TILs include lots of immune cells, such as T cells, B cells, natural killer cells, and macrophages (Kruger et al. 2019). In addition, the antitumor effect of immune cells is being thoroughly studied. CD4+ T cells have been reported to differentiate into various effector cells and can act as helper cells, killing tumor cells through B cells and NK cells. Furthermore, CD4+ T cells can differentiate into T regulatory cells (Tregs), which is critical for maintaining self-tolerance and accomplished by an immunosuppressive mechanism that inhibits the proliferation of other T cells and the production of cytokines (Plitas and Rudensky 2016; Beyar-Katz and Gill 2018). Unlike T cells, NK cells may kill tumor cells by restricting immunoglobulin-like receptors that recognize major histocompatibility class I complexes (Stringaris and Barrett 2017).
A complete immunoglobulin-based artificial immune system algorithm for two-stage assembly flowshop scheduling problem with part splitting and distinct due windows
Published in International Journal of Production Research, 2019
The adaptive immunity consists of two stages: primary and secondary responses. For the primary response, B-cell receptors and T-cell receptors are produced by different combinations of V and J gene segments, named gene rearrangement, in the primary lymphoid organ. Then the B cells will leave the bone marrow and go into the peripheral lymphoid tissue while the T cells will leave the thymus and go into the second lymphoid tissue. By B-cell receptors, B cells capture the pathogen and take it into the nearest peripheral lymphoid tissue. As the circulating B cells pass through the T-cell zones, they make transient interactions that the T cells use its receptors to screen the pathogens presented by the B cells. When the B cells present pathogens recognised by T cells, called cognate interactions, these B cells are subject to somatic hypermutation and isotype switching, and they will eventually produce plasma cells that make high-affinity antibodies of three isotypes, IgG, IgA and IgE, with the help of T cells. However, if the cognate interactions do not happen, only IgM is produced. During a primary response, the pathogen-specific B cells and T cells give rise both to short-lived effector cells that work to stop the infection and to long-lived memory B cells and memory T cells. These memory cells will be easily activated by pathogen to proliferate and differentiate into effector cells. More effective antibodies will be produced to bind and destroy the same pathogen. This stronger and quicker immune response is called secondary response. The details of primary response and secondary response are presented based on the book by Parham (2014).