Immunology Ans.pdf

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University of British Columbia
MICB 202
Tracy Kion

1 MICB 202 – 2011W Immunology Review Questions – Topics 1 and 2. 1. PRRs are receptors on cells of the innate immune responses (or the intracellular vesicles) that recognized “pathogen associated molecular patterns” – these are molecules that are found on the surfaces of pathogens. These molecular patterns are essential to the pathogen and therefore, do not undergo frequent mutation. PRRs may also be found as secreted proteins in the blood/lymph fluids and mucous secretions. Some cell surface PRRs are involved in the binding and phagocytosis of a pathogen by a phagocytic cell. Other cell surface or intracellular PRRs activate signaling pathways upon binding, and result in transcription of cytokine genes. Other soluble PRRs may bind the pathogen and activate the complement cascade (e.g., MBL), and bind a part of the pathogen and transfer it to a signaling PRR (e.g., LBP binding LPS and transferring it to CD14 which ultimately transfers it to TLR4). 2. Person A will have more difficulty fighting an infection as C3 is required earlier in the complement cascade than C5. No C3 will result in: 1. No C3A, a vital inflammatory mediator 2. No C3b based opsonization 3. No C5 convertase, thus resulting in no C5A, another potent inflammatory mediator and chemotaxin, nor C5b, which is required for the assembly of the MAC 3. The newborn mouse would lack mature T cells and thus be unable to initiate either cell mediated or humoral responses against a pathogen. This is because the thymus in a newborn is vital for the proper maturation of T cells. In an adult, who already possesses a vast T cell repertoire against many pathogens, the thymus is not vital and thus its loss would not disrupt the ability of the adult to combat a pathogen. In fact, it is less active and has atrophied. Immunology Review Questions – Topic 3. 4. There are several ways that they are different: Cell distribution. MHC class II is more restricted in its distribution and only on B cells, macrophages, dendritic cells, and some endothelial cells. Structure. MHC class I is made of one polypeptide that non-covalently associates with another. MHC class II is made of two polypeptides. Peptide binding site. MHC class I has its peptide binding site within the chain, MHC class II has its peptide binding site between the chains. Source of peptides. MHC class I peptides are derived from proteins inside the cell’s cytoplasm. MHC class II peptides are derived from outside of the cell, and have been brought into an endocytotic vesicle. Presentation. MHC class I and peptides are usually presented to CD8 T cells, MHC class II and peptides are usually presented to CD4 T cells. Making a table can be a helpful way of answering this question. 2 5. T cells are required to undergo positive selection to ensure that they have the ability to interact with the MHC molecules expressed in the body. The process of creating TCR is random and thus, if the produced TCR cannot recognize MHC, it cannot bind and signal for the activation of that T cell. This makes the T cell useless to the body as it is unable to carry out its function. T cells are required to undergo negative selection to ensure that any self reactive T cells, which could potentially launch an immune response against self antigen, are destroyed. This is required due to the randomness in the process of TCR generation. 6. Signal 1 is the successful binding of the TCR to the proper type of MHC which is displaying the T cells specific antigen as well the successful interaction of CD4 or CD8 with a separate region of the antigen bearing TCR to ensure a proper interaction. Signal 2 is the binding of the costimulatory molecule, B7, on the APC to its receptor, CD28, on the T cell. If only 1 signal is received, the T cell will enter a state of non-responsiveness called anergy. This is to ensure that no unwanted immune responses occur. 7. Dendritic cells interact with T helper cells to activate them. Antibodies made by the adaptive component can opsonize a pathogen, and enhance phagocytosis by a macrophage. Complement proteins (part of the innate system) work with antibodies to kill bacterial pathogens. Later, we will see that T helper 1 cells can activate macrophages that have intracellular infections (so that the macrophage can kill the bacteria). Immunology Review Questions - Topic 4. 8. Antibodies can bind to the surface of the pathogen. Depending on the isotype, this can activate complement, enhance phagocytosis, or neutralize the pathogen. Complement C3b can bind directly to the surface of some pathogens, this can activate the cascade or act as an opsonin. Neutrophils and macrophages can phagocytosis the pathogen, even in the absence of opsonins. The antibodies are made from the adaptive immunity, the others are the innate immunity. 9. Cell mediated responses are required in these cases in order to destroy the bacteria as it has avoided phagocytic killing (it often shuts down the cell’s ability to fuse a lysosome with a phagosome or endosome). It also evades antibodies and/or complement mediated killing because the bacteria is inside a host cell and antibodies and complement cannot cross the membrane of the host cell. A T helper 1 cell is needed to activate the macrophage that has an intracellular infection, so that the macrophage can then mount a more aggressive response to kill the bacteria. 10. No. Both humoral (Ab) and cell-mediated immunity is occurring. If an antibody can neutralize a virus before it can infect a cell, the cell remains healthy and functional; furthermore, that cell is saved from killing by CTLs. 11. It is more appropriate to develop an antibody response when the pathogen is outside of the cell. The Ab can block it and prevent it from binding to the cell or entering the cell. Once the pathogen is inside of the cell, Ab are not able to act against it. Therefore, a cell-mediated response is needed to kill the pathogen (unfortunately, it also kills the cell that has the pathogen inside it). 3 12. Only an antibody response is expected. Since the virus is inactivated, it cannot bind and infect cells. Therefore, no viral proteins are being synthesized and expressed on MHC class I molecules. Immunology Review Questions - Topic 5. 13. Hypersensitivity = exaggerated immune responses (humoral and cell mediated) that result in damage to the individual. Often, these inappropriate responses are to antigens that are not really harmful to the body. There are two subclasses discussed in the course notes. Immediate hypersensitivity occurs within minutes of exposure to the antigen, it is also referred to as an allergy. Delayed type hypersensitivity occurs in about 2 or 3 days after exposure to the antigen. Immediate type hypersensitivity (ITHS) is dependent on mast cells and the production of IgE specific for a substance (allergen). It is not known why some people create IgE against harmless substances only that certain people will favor IgE responses against certain substances. ITHS only occurs after the primary response. B cells specific to the allergen expand, creating a large pool of cells specific to the allergen. Some of these cells will have isotype switched to IgE. Even when an immunogenic substance is not present, antibodies against it are made at low levels. The antibodies in this case, IgE, bind to receptors found on mast cells. When the allergen is present again, it binds to IgE on the mast cells, which triggers the mast cells to release their stores of histamine, a potent inflammatory mediator. This results in a strong inflammation. DTHS is dependent on T helper 1 cells and their activation of macrophages. In this type of HS, the body is exposed to a material, a hapten, which readily passes through the skin. Once through, they bind to self peptides, altering their conformation. Resident Langerhans cells (a type of dendritic cell) take up these materials and migrate to lymph nodes where they drive the expansion of T helper 1 cells specific for the hapten:peptide complex. Memory cells are produced. When the offending substance is encountered again, these memory cells become active and migrate to the site of the exposure. Once there, they activate tissue macrophages, resulting in a potent immune response. Both DTHS and ITHS are dependent on the adaptive immune system as well as the innate. They both only occur during
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