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Basic Chemical Hazards to Human Health and Safety — II
Published in Jack Daugherty, Assessment of Chemical Exposures, 2020
The lymphocytes that produce cellular immunity are called T-cells, which attack only those antigens that have been processed by other cells. Phagocytes engulf antigens and break them down. The cell fragments and proteins from the infection agent are displayed on the surface of the phagocyte, bound by cell surface proteins called human leukocyte antigen proteins, produced by genes called the major histocompatibility complex, which are unique markers that identify self from nonself. T-cells respond to the HLA protein and foreign antigen combination in a molecular lever lock and key fashion. Killer T-cells secrete a cytotoxic substance to destroy antigens. Memory T-cells are dormant until the same antigen reappears, then they attack swiftly. Helper T-cells promote T-cell activation, stimulate phagocytic activity, and enhance the humoral immunity process. Suppressor T-cells produce delayed inhibition of cellular and humoric responses.
Immunotherapy and Vaccines
Published in Raj Bawa, János Szebeni, Thomas J. Webster, Gerald F. Audette, Immune Aspects of Biopharmaceuticals and Nanomedicines, 2019
Johanna Poecheim, Gerrit Borchard
In the course of the adaptive immune response to infection, clones of pathogen-specific B and T cells spread as effector cells. Additionally, long-lived clones of memory T cells that form the immunological memory are produced. Subsequent immune responses to the same pathogen will be faster and stronger, since memory cells are more quickly activated than naive cells. Unlike naive T cells, memory T cells can patrol nonlymphoid tissues, such as mucosae, and detect infection at an earlier stage. The greater power of a secondary immune response supports the generation of vaccine-mediated protection. By applying antigenic structures of the pathogen to the body without inducing the disease, immunological memory is elicited. Additionally, Th1- and Th2-polarizing adjuvants may be introduced to direct the desired immune response (Parham, 2000; Plotkin et al., 2013).
Development and Application of Phase Change Materials in the Biomedical Industry
Published in Atul Sharma, Amritanshu Shukla, Renu Singh, Low Carbon Energy Supply Technologies and Systems, 2020
Abhishek Anand, Amritanshu Shukla, Atul Sharma
The WBCs play an important role in the immune response. WBCs come in various shapes and sizes. Some cells have a nucleus with lobes, and others have one single round nucleus. WBCs can be classified into three types: granulocytes, monocytes, lymphocytes. Granulocytes have granules in the cytoplasm. They account for 60% of our WBCs. They engulf and destroy invading bacteria and viruses. Granulocytes are further divided into neutrophils, eosinophils, and basophils. Neutrophils are the main phagocytes. They are the first responders to the site of any inflammation. Eosinophils are involved in allergic reactions and asthma. They kill multicellular organisms, particularly worms. Basophils are about 0.5%–1% of the total WBCs. They are concerned with allergic reactions. They release histamine and serotonin that augments inflammation. They also release heparin, which prevents blood from clotting. Monocytes are divided into dendritic cells and macrophages. Dendritic cells (DCs) are the antigen-presenting cells. DCs can point out foreign cells that have to be destroyed by the lymphocytes. Macrophages destroy and engulf foreign cells in the process called phagocytosis. Lymphocytes are also the body’s immune cells, which are categorized into B lymphocytes (B cells) and T lymphocytes (T cells). Both B cells and T cells originate from stem cells in the bone marrow. Some travel to the thymus, where they convert to T cells, and others stay in the bone marrow, where they become B cells. B cells release antibodies that are Y shaped and bind to the infected cells or microbes. It offsets the target microbes or smears it to be attacked by T cells. T cells are further categorized into helper T cells, cytotoxic T cells, memory T cells, and regulatory T cells. Helper T cells release cytokines that facilitate other WBCs. Cytotoxic T cells kill viruses and other cancerous cells. The memory T cell is an experienced cell because of a previous infection or vaccination. During a later encounter, it can generate a superior immune response. Regulatory T cells stop other T cells from earmarking body cells.
A mathematical model of cytotoxic and helper T cell interactions in a tumour microenvironment
Published in Letters in Biomathematics, 2018
Heidi Dritschel, Sarah L. Waters, Andreas Roller, Helen M. Byrne
We assume that the evolution of the helper and cytotoxic T cells is dominated by infiltration from the lymph nodes, proliferation in response to the tumour cells and natural cell death. We assume that the two T cell populations infiltrate the tumour from the lymph nodes at constant rates and (units: number of cells day), and die at rates and (units: day). Naive T cells are regularly produced by hematopoietic stem cells and therefore a constant population of these naive T cells are present in the circulating blood stream. We can assume that the flow of blood is constant and therefore, in addition to direct stimulation of T cells in the presence of tumour antigen, there is a constant influx of primed T cells from the circulating blood. Furthermore, this assumption enables us to implicitly account for the presence of a constant pool of memory T cells present in the absence of antigen stimulation (Farber et al., 2014). This approach has been widely adopted in similar models to account for a background level of circulating T cells (de Pillis et al., 2005; Eftimie et al., 2011; Kuznetsov et al., 1994).
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).