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21 Cards in this Set
- Front
- Back
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Lymphatic capillaries |
Lymphatic capillaries more permeable than systemic capillaries, composed of a series of one way valves. The capillaries are made of a series of epithelial cells which overlap - they open when there's no lymph inside, allowing fluid to flow in, and close to generate pressure when there's movement due to skeletal muscle, pushing the lymph forward through the valves. They are capped shut at one end. |
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Functions of lymphatic system |
1. Defense: pathogens are swept up by lymph, carried to lymph node sand lymphatic nodules where macrophage and lymphocyte concetrations are high 2. Drains excess fluid. If vessels are blocked, forms lymphedema, irreversible large scale swelling due to collected fluid in tissue 3. Fat absorption and digestion from ingested food |
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Lymphatic nodules+lymph nodes |
Similar in function but different in structure. They both have lymphocytes and macrophages to aid in defense. Lymhatic nodules are enlarged regions of lymphatic capillaries, whereas lymph nodes are located where many lymphatic vessels converge. Lymph nodes have many afferent vessels feeding and one efferent vessel draining out at the hillous. The hillous also has an arteriole and venule, providing transportation for immune cells to travel and reside in the lymph node. Setpa divide he lymph node, and dense patches house the immune cells. Lymph nodes are concentrated in external/internal boundaries, such as the mouth, which as 3 groups, the palatine, pharyngeal, and lingual lymph tissue.
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Drainage of the lymphatic system |
Drains asymmetrically - the lower half of the body and the left upper half drain into the thoracic duct, which drains into the left subclavian vein, while the upper right half of the body drains into the right lymphatic duct. All of the lymph is returned to general circulation through veins, which are returned into the superior vena cava |
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Thymus gland |
Located on top of the aorta, it does not grow with the rest of the body with age. It is separated into lobules by septa, with a thymic corpuscle in the center of the medulla region with an unknown function. T lymphocytes mature in the thymus gland after being made in the bone marrow before either staying in the blood or migrating to take residence in tissues. By contrast, B lymphocytes are produced and mature in the bone marrow. |
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Innate immune response |
The same, general sequence of defense mechanisms regardless of the trigger, acting as the body's first line of defense: Mechanical mechanisms prevent entry of and remove foreign objects. White blood cells phagocytose Neutrophils and macrophages ingest and break down NK cells chemically kill Mast cells and basophils promote the inflammatory response Eosinophils reduce inflammation post response and promote tissue repair |
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Adaptive/specific immunity |
The body learns to recognize and respond to specific invaders. It has specificity, the ability to recognize particular substances, and memory, the ability to remember particular substances and rapidly respond to them. Adaptive immunity involves antibodies, B and T lymphocytes. |
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Sentinel cells |
Part of the innate immune response Sentinel cells has toll like receptor dimers that recognize for common molecular patterns on the invader cell surface that are not present in own cells, such as double stranded RNA. It will secrete cytokines and prostaglandins to promote inflammation, and will also recruit macrophages via chemotaxis. |
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Interferon |
Part of the innate immune response If a cell becomes aware that it is infected, it will secrete interferon alpha, attracting immune cells and binding to neighbouring cells to inhibit their receptor production, making them resistant to viruses |
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Natural Killer cells |
Part of the innate immune response Natural killer cells check for the correct pattern and ratio of antigenic determinants with its antigenic receptors, binding itself to invading cells. The golgi of the NK cell migrates to face the invading cell and secretes perforin, whose subunits insert themselves into the invading cell membrane and polymerize for form a large pore and disrupt homeostasis. |
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Complement cascade |
Part of the innate response, it has two pathways. The classical arm relies on antibodies made from a previous encounter with the specific invader, which will provide a scaffold for C1 protein to bind. C1 works on C2 and C4, making an enzyme that cuts C3 in half. C3a attracts WBCs via chemotaxis, while C3b works on C5-C9, producing a membrane attack complex that forms a pore in the outer boundary of the invading cell, disrupting osmoregulation and forcing excess water into the cell to cause lysis.The alternate pathway is able to accomplish the same thing without the use of antibodies. It instead relies on properidin factor B, and factor D that recognize unusually complex carbohydrate side chains on glycoproteins only present in prokaryotes, before binding to the side chains and forming the enzyme that will cut C3 and eventually make the MAC. |
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Inflammation |
The first step of the innate immune response.The inflammatory response is a result of cells releasing mediators such as histamine, which results in three responses all designed to bring more WBCs to the area:1. Dilation of precapillary sphincters to open a pathway2. Opening of larger intracellular clefts between endothelial cells to make them more vessel walls more permeable3. Attraction of immune cells via chemotaxis.If the WBCs succeed in killing the invader, tissue repair can begin. If not, additional chemical mediators are activated and trigger a positive feedback cycle to recruit more WBCs. |
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Major histocompatibility complex |
MHCs are divided into 2 classes, class I is present on all nucleated cells, while class II are only present on immune phagocytic and B cells. The mHC is expressed on glycoproteins, and requires a fragment of antigen within it to form the correct shape to function. MHCs will pick up bits of protein being produced in the cell during its own production process before being exocytosed in a vesicle to the surface of the cell, where it presents the antigen to be inspected. If a virus infects a cell, the MHC will pick up the viral protein being produced and present it to immune cells |
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T cell maturation |
Produced in the bone marrow, T cells migrate to the thymus gland to mature, moving gradually from inwards towards the medulla of a lobule in the process. T cells rely on T cell receptors to recognize antigens, and the gene for TCRs are separated into 3 parts: a constant part, several joining regions, and several variable regions. An enzyme slopily grabs the region between any V and any J region, wrapping it up into a loop and destroying it. Thus, depending on where the enzyme grabs, and number of V and J regions can be destroyed. The remaining V and J regions closest to where the enzyme grabs is joined up, and depending on where the enzyme grabs, any combination can be joined, this permanently sets the structure. When the cell is transcribed from C, which holds the promotor, to J to the first V holdin the terminator sequence, the primary transcript is modified, cutting out all of the J regions as introns except for the one joined to the V. The finished transcript codes for the alpha TCR subunit, which binds with a constant beta TCR subunit. The differing alpha subunits allow for different TCRs to be made Thus different T cells are able to recognize different antigenic factors - the human body is immune to everything in very small amounts, and exposure increases the number of T cells specific to that invader, raising immunity for against specific antigen pattern. |
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Immune cell testing |
Beta selection: Because the alpha subunit of TCRs are so sloppily made, it may not be able to combine with the beta subunit. If it can't, it will be destroyed. Positive selection: Cells around the maturing T cell will have MHCs displaying a very small piece of self antigen, too small to be recognized. T cells will be tested to see if they will bind or not. If it cannot bind to the MHC with its TCR, it is destroyed At this point, T cells are differentiated based on their affinity for the two MHC classes. If it binds easily with MHC class I, it becomes a CD4 T cell, MHC class II becomes CD8. Negative selection: At this point, MHC cells present another self antigen, this time large enough to be recognizable. If the T cells bind to them, it will be destroyed. B cells undergo a similar selection process without the positive selection step |
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How a T cell attacks invading cells |
There are 3 classes of T cells: CD4 (helper) T cells that look for professional APCs and screen of antigens Regulatory (Treg) cells that suppress the immune response and prevent a positive feedback loop. When a cell becomes infected, it releases cytokines to attract lymphocytes. The naive T cells go around binding with all cells, but are unable to bind to cells with the MHC expressing self antigens. When it gets to an MHC expressing an antigen that isn't self but is also recognizable to that specific T cell's specific TCR, it will bind to it, becoming chemically activated. The activation will cause the T cell to fall off and undergo rapid mitosis, producing daughter cells that can code for the TCR to recognize that antigen. Some daughter cells (20%) remain quiescent as memory cells, while the rest go hunt for the infected cell with MHCs displaying the correct antigen. The daughter cells will bind and release lymphotoxins to disrupt metabolism, cytokines to promote apoptosis, and perforin to disrupt osmoregulation |
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Professional APCs and costimulatory signal |
Certain cells are specifically designed to present antigens, called professional antigen presenting cells. Only these cells are capable of producing a costimulatory signal (necessary to help prevent autoimmunity), an example of which is the B7 protein on the professional APC interacting with the CD28 on helper T cells |
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How helper T and B cells function
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Macrophages phagocytose either the body or invading pathogen's dead cell bits. The vesicle that's formed fuses with lysosomes that contain empty MHC II containers. As the cell bits get broken down, antigens get picked up by the MHC II and exocytosed to the cell's surface. If a naive CD4 has the correct TRC and CD28, it will bind with the macrophage displaying the MHC II and B7 activate, causing it to fall off and undergo rapid mitosis. Some stay quiescent while other seek out B cells with the same processed antigen receptors. B cells process antigens much like macrophages, and if a correct CD4 binds with the correct B cell, the B cell will get activated and fall off to undergo mitosis. Some stay quiescent while the rest produce antibodies, are identical in structure to the center of their B cell receptor
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Antibody functions |
Antibodies are made complimentary to antigens and are able to bind to foreign entities. They can... 1. Block invaders from binding to anything else (e.g. viruses binding to body cells) 2. Clump invaders together by attaching to them and then interlinking with each other, this stimulates phagocytosis by macrophages. 3. Activates the classical arm of the complement cascade 4. Activates mast cells and basophils to initiate the inflammatory response |
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Immune response variations |
Bacterial infection damages tissues, which activates macrophages --> CD4 --> B cells --> antibodies Viral infections activate NK cells, a more innate rather than adaptive response Vaccines contain weakened pathogen or viral proteins that provide artificial exposure and induces adaptive immunity. Passive immunity is immunity that's transferred from another person or animal, such as from the mother via placental uptaking, or purified from other animals, such as the anti Rh antibody |
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Effect of aging on the lymph+immune systems |
The lymphatic system is not affected strongly by aging. The thymus gland slows with age, causing a decreased ability to produce new T cells. This results in naive T cells dividing to replicate instead of novel ones being made, which decreases primary and secondary antibody response systems and the effectiveness in cell mediated immunity |
