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NCSU MB 441 - Study Guide for Exam 1 (Lectures 1-4)

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Study Guide for Exam I (Lectures 1-4)Pathogenic organisms are of four main types - viruses, bacteria, fungi, and parasites.Our immune defenses begin at the epithelium. Barriers to infection on this surface can be divided into three categories: mechanical, chemical, and microbiological. One mechanical barrier to infection common to all epithelial surfaces is the joining of cells via tight junctions, which leaves no extracellular space through which pathogens can enter. Alternatively, epithelial surfaces constantly experience a flow of fluid, such as perspiration, mucus or food, that prevent pathogens from accumulating at a particular region of the epithelium. Chemical barriers to infection include the release of antimicrobial peptides called defensins as well as lysozyme – an enzyme common to tears, saliva and mucus that attacks peptidoglycans in bacterial cell walls. The creation of an acidic environment, such as that found in the stomach, is also a chemical barrier to infection. Microbiological barriers to infection consist of the normal flora present at each epithelial surface, which leave no room for colonization. Unlike infectious microorganisms, our normal flora is not pathogenic andwill not cause disease under normal circumstances. Almost all components of the immune system contribute to mechanisms for either detecting or removing pathogens.When the epithelium is penetrated, usually the first step is to induce inflammation. Resident effector cells called macrophages (“large eaters”) can phagocytose or engulf invading pathogens as well as secrete inflammatory chemicals called cytokines. Inflammation assists the immune response in four ways: slowing pathogen spread, slowing pathogen growth, recruiting immune cells, and initiating the adaptive immune response. Innate and adaptive immunity have common effector mechanisms for destroying pathogens, but differ substantially in other ways. Innate immunity responds rapidly, in a fixed way, reacting to a limited number of specificities and its effectiveness is constant during the response. Adaptive immunity responds slowly, in variable ways, reacting to a massive number of specificities and its effectiveness improves during the response. In normal individuals, a primary infection is cleared from the body by the combined effects of innate and adaptive immunity. In a person who lacks innate immunity, uncontrolled infection occurs because the adaptive immune response cannot be deployed without the preceding innate response. In a person who lacks adaptive immune responses, the infection is initially contained byinnate immunity but cannot be cleared from the body.All cells of the immune system come from a single progenitor - the hematopoietic stem cell, which differentiates into cells of the lymphoid lineage, the myeloid lineage, and the erythroid lineage. Cells of the lymphoid lineage include B cells, T cells, and NK cells. Cells of the myeloid lineage include monocytes, which give rise to dendritic cells and macrophages resident in tissues, neutrophils and eosinophils, basophils and mast cells, which we will discuss later for their involvement in allergies and autoimmune diseases.Neutrophils and lymphocytes represent the vast majority of the leukocytes in our bloodstream. After one round of ingestion and killing of bacteria, a neutrophil dies, forming pus. These are eventually mopped up by long-lived macrophages, which break them down. Bacteria binds to cell-surface receptors on macrophages, inducing engulfment of the bacterium into an internal vesicle called a phagosome within the macrophage cytoplasm. Fusion of this phagosome with lysosomes forms an acidic vesicle called a phagolysosome, which contains toxic small molecules and hydrolytic enzymes that kill and degrade the bacterium. Bacterial components binding to a different typeof cell surface receptor sends a signal to the macrophage's nucleus that initiates the transcription of genes for inflammatory cytokines. Specialized phagocytes called dendritic cells transport ingested pathogens to secondary lymphoid tissues to begin an adaptive immune response.Lymphocytes arise from stem cells in the bone marrow. B cells complete their maturation in the bone marrow, whereas T cells leave at an immature stage and complete their development in the thymus. The bone marrow and the thymus are the primary lymphoid tissues. Secondary lymphoid tissues include thetonsils, spleen, appendix and myriad lymph nodes scattered throughout the body.Lymphocytes are unique among blood cells in traveling through the body in the lymph as well as the blood. Lymphocytes leave the blood through capillaries in secondary lymphoid organs such as lymph nodes. There they interact with lymph – packed with pathogens and pathogen-laden dendritic cells during an infection – which arrives in lymph nodes via the afferent lymphatic vessels, percolates for awhile among lymphocytes brought from the blood, then leaves via the efferent lymphatic vessels. If a lymphocyte does not encounter pathogen, it returns to the blood. However if a lymphocyte in a lymph node encounters a pathogen to which its cell-surface receptor binds, it stays in the lymph node to divide and differentiate into effector cells. Within the lymph node, B cells and T cells tend to congregate in anatomically discrete areas. T cells populate the inner cortex and B cells form lymphoid follicles in the outer cortex. During an infection, the expansion of pathogen-specific B cells forms a spherical structure called a germinal center within each follicle. The spleen is a large abdominal secondary lymphoid organ responsible for filtering pathogens from the blood. Infections in the blood system that are not promptly cleared can lead to septic shock, which can quickly result in widespread organ failure and death. Adaptive effector cells play different roles after responding to pathogen in a lymph node. Some helper T cells and cytotoxic T cells leave in the efferent lymph and travel to the infected tissue via the lymph and blood to boost macrophage activity and kill virus-infected cells, respectively. Other helper T cells remain in the lymph node and stimulate the division and differentiation of pathogen-specific B cells into plasma cells. Plasma cells move to the medulla of the lymph node, where they secrete pathogen-specific antibodies, which are taken to the site of infection by the efferent lymph and subsequently the blood.


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NCSU MB 441 - Study Guide for Exam 1 (Lectures 1-4)

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