BIOL235 FINAL REVIEW BEST GUIDE 2021 |ATHABASCA UNIVERSITY

BIOL235 FINAL REVIEW BEST GUIDE 2021 |ATHABASCA UNIVERSITY BIOL235 FINAL REVIEW BEST GUIDE 2021 |ATHABASCA UNIVERSITY BIOL235 FINAL REVIEW BEST GUIDE 2021 |ATHABASCA UNIVERSITY BIOL235 FINAL REVIEW BEST GUIDE 2021 |ATHABASCA UNIVERSITY 8. Compare the functions of cell mediated immunity and antibody mediated immunity. A. antigens (Ags) and antigen receptors: have two important characteristics: immunogenicity and reactivity. B. Immunogenicity: is the ability to provoke an immune response by stimulating the production of specific antibodies, the proliferation of specific T cells, or both. C. Reactivity: is the ability of the antigen to react specifically with the antibodies or cells it provoked. Strictly speaking, immunologists define antigens as substances that have this trait D. complete antigens: substances with both immunogenicity and reactivity are considered E. Epitopes: Typically, just certain small parts of a large antigen molecule act as the triggers for immune responses. Most antigens have many of these, each of which induces production of a specific antibody or activates a specific T cell. F. Hapten: A smaller substance that has reactivity but lacks immunogenicity. They can stimulate an immune response only if it is attached to a larger carrier molecule. An example is the small lipid toxin in poison ivy, which triggers an immune response after combining with a body protein. Likewise, some drugs, such as penicillin, may combine with proteins in the body to form immunogenic complexes. Such hapten-stimulated immune responses are responsible for some allergic reactions to drugs and other substances in the environment G. major histocompatibility complex (MHC) antigens: These transmembrane glycoproteins are also called (HLA). Unless you have an identical twin, these antigens are unique. Thousands to several hundred thousand of these molecules mark the surface of each of your body cells except red blood cells. Although these antigens are the reason that tissues may be rejected when they are transplanted from one person to another, their normal function is to help T cells recognize that an antigen is foreign, not self. Such recognition is an important first step in any adaptive immune response. H. pathways of antigen processing: For an immune response to occur, B cells and T cells must recognize that a foreign antigen is present. B cells can recognize and bind to antigens in lymph, interstitial fluid, or blood plasma. T cells only recognize fragments of antigenic proteins that are processed and presented in a certain way. In antigen processing, antigenic proteins are broken down into peptide fragments that then associate with MHC molecules. Next the antigen–MHC complex is inserted into the plasma membrane of a body cell. The insertion of the complex into the plasma membrane is called antigen presentation. When a peptide fragment comes from a self-protein, T cells ignore the antigen–MHC complex. However, if the peptide fragment comes from a foreign protein, T cells recognize the antigen–MHC complex as an intruder, and an immune response takes place. Antigen processing and presentation occur in two ways, depending on whether the antigen is located outside or inside body cells. I. antigen presenting cells (APCs): process and present exogenous antigens. APCs include dendritic cells, macrophages, and B cells. They are strategically located in places where antigens are likely to penetrate the innate defenses and enter the body, such as the epidermis and dermis of the skin (intraepidermal macrophages are a type of dendritic cell); mucous membranes that line the respiratory, gastrointestinal, urinary, and reproductive tracts; and lymph nodes. After processing and presenting an antigen, APCs migrate from tissues via lymphatic vessels to lymph nodes. 1) Ingestion of the antigen. Antigen-presenting cells ingest exogenous antigens by phagocytosis or endocytosis. Ingestion could occur almost anywhere in the body that invaders, such as microbes, have penetrated the innate defenses. 2) Digestion of antigen into peptide fragments. Within the phagosome or endosome, protein- digesting enzymes split large antigens into short peptide fragment 3) Synthesis of MHC-II molecules. At the same time, the APC synthesizes MHC-II molecules at the endoplasmic reticulum (ER). 4) Packaging of MHC-II molecules. Once synthesized, the MHC-II molecules are packaged into vesicles. 5) Fusion of vesicles. The vesicles containing antigen peptide fragments and MHC-II molecules merge and fuse. 6) Binding of peptide fragments to MHC-II molecules. After fusion of the two types of vesicles, antigen peptide fragments bind to MHC-II molecules. 7) Insertion of antigen–MHC-II complexes into the plasma membrane. The combined vesicle that contains antigen– MHC-II complexes undergoes exocytosis. As a result, the antigen–MHC-II complexes are inserted into the plasma membrane. After processing an antigen, the antigen-presenting cell migrates to lymphatic tissue to present the antigen to T cells. Within lymphatic tissue, a small number of T cells that have compatibly shaped receptors recognize and bind to the antigen fragment– MHC-II complex, triggering an adaptive immune response. The presentation of exogenous antigen together with MHC-II molecules by antigen-presenting cells informs T cells that intruders are present in the body and that combative action should begin. J. endogenous antigens: Foreign antigens that are present inside body cells. Such antigens may be viral proteins produced after a virus infects the cell and takes over the cell’s metabolic machinery, toxins produced from intracellular bacteria, or abnormal proteins synthesized by a cancerous cell. 1) Digestion of antigen into peptide fragments. Within the infected cell, protein-digesting enzymes split the endogenous antigen into short peptide fragments. 2) Synthesis of MHC-I molecules. At the same time, the infected cell synthesizes MHC-I molecules at the endoplasmic reticulum (ER). 3) Binding of peptide fragments to MHC-I molecules. The antigen peptide fragments enter the ER and then bind to MHC-I molecules. 4) Packaging of antigen–MHC-I molecules. From the ER, antigen–MHC-I molecules are packaged into vesicles. 5) Insertion of antigen–MHC-I complexes into the plasma membrane. The vesicles that contain antigen–MHC-I complexes undergo exocytosis. As a result, the antigen–MHC-I complexes are inserted into the plasma membrane. Most cells of the body can process and present endogenous antigens. The display of an endogenous antigen bound to an MHC-I molecule signals that a cell has been infected and needs help. K. Cytokines: are small protein hormones that stimulate or inhibit many normal cell functions, such as cell growth and differentiation. Lymphocytes and antigen-presenting cells secrete them, as do fibroblasts, endothelial cells, monocytes, hepatocytes, and kidney cells. Some stimulate proliferation of progenitor blood cells in red bone marrow. Others regulate activities of cells involved in innate defenses or adaptive immune responses, 9. Outline the steps in a cell mediated immune response. A. cell mediated immunity: begins with activation of a small number of T cells by a specific antigen. Once a T cell has been activated, it undergoes clonal selection. The result of clonal selection is the formation of a clone of cells that can recognize the same antigen as the original lymphocyte. Some of the cells of a T cell clone become effector cells, while other cells of the clone become memory cells. The effector cells of a T cell clone carry out immune responses that ultimately result in elimination of the intruder. I. activation, proliferation and differentiation of T cells: The need for two signals to activate a T cell is a little like starting and driving a car: When you insert the correct key (antigen) in the ignition (TCR) and turn it, the car starts (recognition of specific antigen), but it cannot move forward until you move the gear shift into drive (costimulation). The need for costimulation may prevent immune responses from occurring accidentally. Different costimulators affect the activated T cell in different ways, just as shifting a car into reverse has a different effect than shifting it into drive. II. T cell receptors: recognize and bind to specific foreign antigen fragments that are presented in antigen–MHC complexes. III. Costimulation: A T cell becomes activated only if it binds to the foreign antigen and at the same time receives a second signal. Of the more than 20 known, some are cytokines, such as interleukin-2 (IL-2). Others include pairs of plasma membrane molecules, one on the surface of the T cell and a second on the surface of an antigen-presenting cell, that enable the two cells to adhere to one another for a period of time. IV. interleukin 2: a cytokines co stimulator. It is needed for virtually all immune responses and is the prime trigger of T cell proliferation. IL-2 can act as a costimulator for resting helper T cells or cytotoxic T cells, and it enhances activation and proliferation of T cells, B cells, and natural killer cells. Some actions of interleukin-2 provide a good example of a beneficial positive feedback system. V. Anergy: Moreover, recognition (antigen binding to a receptor) with- out costimulation leads to a prolonged state of inactivity. is rather like leaving a car in neutral gear with its engine running until it’s out of gas! .................................CONTINUED*.............................