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Bio — 6.3
immune system
| Question | Answer |
|---|---|
| zoonosis | disease which can be transmitted to humans from animals (e.g. rabies, west nile virus) |
| antibody | compound/protein produced by B lymphocytes (and plasma cells) that kills or inhibits growth of microbes (specifically bacteria) by targeting prokaryotic metabolism; specific to a given antigen |
| antigen | substance that the body recognizes as foreign and that will elicit an immune response |
| active immunity | results from production of antibodies by immune system in response to presence of an antigen (primary immune response) |
| passive immunity | short-term immunity which results from introduction of antibodies from another person, animal, or other organism |
| skin | - protects external structures - dry, thick, tough region of dead surface cells - glands secrete chems and enzymes that restrict bacterial growth - secretes lactic acid and fatty acids to lower pH |
| mucus membrane | - protects internal structures & cavities - thin region composed of living cells that secrete fluid (mucus, saliva, tears) to trap pathogens - biochemical defense agents (e.g. lysozyme) - cilia to remove pathogens |
| blood clots | - clotting is the mechanism by which broken blood vessels are repaired - clotting prevents blood loss from the body and limit pathogenic access to the bloodstream when the skin is broken |
| components of blood clots | - platelets→ undergo a structural change to form a sticky plug at the damaged region - fibrin strands→ form an insoluble mesh of fibers that trap blood cells at damaged region |
| clotting factors --> causes | - cause platelets to become sticky and adhere to the damaged region to form a solid plug (clot), sealing wound - trigger the conversion of the inactive prothrombin into the activated enzyme thrombin |
| clotting factors --> enzymes | - thrombin catalyses the conversion of soluble fibrinogen into insoluble fibrin - when the damaged region is completely repaired, plasmin is activated to dissolve the clot |
| clotting factors --> consequences | - process of events is called a coagulation cascade - clot formation in coronary arteries lead to heart attacks |
| pathogen | disease-causing agent that disrupt the normal physiology of infected organisms (i.e. homeostatic imbalance) |
| antibiotic | - compounds that target prokaryotic features but don’t harm eukaryotic cells (i.e. don’t affect host organism) - some bacteria strains have evolved with genes that confer resistance to antibiotics (some even have multiple resistance) |
| antibiotic limitation | can’t be used to treat viruses as they are not alive (no metabolism) |
| first line of defense | surface barriers (skin/mucus) |
| second line of defense | innate immunity (non-specific) |
| third line of defense | adaptive immunity (specific) |
| innate immunity characteristics | - non-specific (i.e. do not differentiate between different types of pathogens) - non-adaptive (i.e. produce the same response to every infection – there is no immunological memory) |
| phagocytosis | - process by which solid materials (such as pathogens) are ingested by a cell - damaged tissues release chemicals (e.g. histamine) which draw white blood cells to the site of infection |
| phagocytosis --> engulf | - pathogens are engulfed by white blood cells - vesicle formed is fused to a lysosome to digest pathogen - antigens may be presented on surface of phagocyte in order to stimulate third line of defense |
| adaptive immunity characteristics | - specific (i.e. can differentiate between different types of pathogens and respond accordingly) - adaptive (i.e. produce a heightened response upon re-exposure – there is immunological memory |
| lymphocyte | - makes a one specific type of antibody - need a lot of Rough ER to transport antibodies |
| B-cell activation | - macrophage consumes virus and displays antigen on its surface -helper T cells bind to macrophages and are activate - helper T cells then release cytokines to activate particular B cell capable of producing antibodies specific to antigen |
| activated B cell actions | - divide and differentiate to form short-lived plasma cells that produce high amounts of specific antibody - antibodies that attach to the antigens will promote the destruction |
| antibodies --> solubility (1st stage) | soluble pathogens become insoluble, which will mark pathogens for phagocytes to destroy them |
| antibodies --> clumping (2nd stage) | cellular pathogens become clumped for easier removal |
| antibodies --> toxins (3rd stage) | neutralize toxins which are produced by the pathogen |
| antibodies --> binding (4th stage) | binds to plasma membrane of a pathogen which breaks down cell membrane and cytoplasm will leak out→ kills pathogen |
| memory lymphocytes | some lymphocytes will remain after the destruction of the pathogen and persist as memory cells |
| HIV & AIDS | - Human Immunodeficiency Virus (HIV) is a retrovirus that infects helper T cells, disabling the body’s adaptive immune system - causes a variety of symptoms and infections collectively classed as Acquired Immunodeficiency Syndrome (AIDS) |
| HIV steps --> T-helper cells | - T-helper cells have a protein called CD4 on the surface of the cell - virus will attach to the CD4 of the T-helper cell and inject RNA, enzymes reverse transcriptase and integrase |
| HIV steps --> enzymes | - reverse transcriptase: creates DNA from mRNA - integrase: will integrate the viral DNA with the host DNA |
| HIV steps --> production of viruses | T-helper cell will begin to produce viruses and these viruses will go and continue to damage T-helper cells (this could take years→ that’s why you may HIV but not AIDs) |
| HIV transfer | - small tears or cuts in vagina, penis, mouth, or intestine during oral, vaginal, or anal sex - sharing of needles - breastfeeding, childbirth |
| effects of HIV | - reduction in the number of helper T cells→ antibodies are unable to be produced→ lower immunity - body becomes susceptible to opportunistic infections, eventually resulting in death if condition is not managed |
| HIV prevention | Antiretroviral Drugs can prevent reverse transcriptase from working |
| antibiotics --> prokaryotic features | key enzymes, 70S ribosomes and components of the cell wall |
| antibiotics --> eukaryotic features | eukaryotic cells do not possess these features→ antibiotics will target the pathogenic bacteria and not host |
| antibiotics --> actions | may either kill the invading bacteria or suppress its potential to reproduce |
| penicillin | first chemical compound found to have antibiotic properties |
| Florey and Chain’s experiment | - 8 mice were injected with hemolytic streptococci - 4 of these mice were then injected with doses of penicillin - untreated mice died of bacterial infection and the others survived→ demonstrates antibiotic potential |
| monoclonal antibodies | - antigen if injected into mouse→ produces B-cells - B-cells are extracted - nucleus of B-cell will be fused into a tumour cell→ this is called a hybridomas |
| monoclonal antibodies --> hybridomas | - hybridomas will divide without control and all the new cells formed can produce thespecific antibodies - antibodies are extracted and are called monoclonal antibodies |
| monoclonal antibodies --> pregnancy tests | - pregnancy tests contain a monoclonal antibody that binds to HCG - HCG is hormone found in the urine of pregnant woman - if monoclonal antibody binds to HCG→ produces a positive line |
| monoclonal antibodies --> usage in treatment | - injection of monoclonal antibodies into person infected with rabies - target cancer cells that the body’s own immune cells fail to recognize as harmful |
| vaccination | - contains a weakened form of a microorganism - body responds by initiating a primary immune response, which results in memory cells being made |
| vaccination --> memory cells | - memory cells allow for a quicker and more potent secondary immune response - causes a bit of antibodies to be produce and some memory cells are produced - second shot→ allows for a faster and greater production of antibodies |