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67 Cards in this Set
- Front
- Back
What recognizes MHC1? What does it say?
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Cytotoxic T cells and NK cells
"I am a cell that belongs in your body and we are unique" |
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Where are MHC 1s found?
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All cells except RBC
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What do MHC1s bind with?
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Virus infected cells, non self cells or abnormal self cells
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What do MHC2 cells do?
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Antigen presenting and activate adaptive immunity
Found on Antigen Presenting Cells: macrophages, dendritic cells and B cells |
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What recognizes the MHC2 cells? What do they bind with?
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T helper cells
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What does the helper T cell do?
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Detects the antigen on the MHC2 and activates either the B or T cell response
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What happens when a helper T cell initiates a B cell response?
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Has to find the B cell with the complementary B cell with the right receptor, triggering to make many copies of itself. One set is banked as a memory cell in the lymphatic system. Others are effectors, undergoing final differentiation to create plasma cells. Terminal differentiation to secrete fighting antibodies.
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What happens when a helper T cell initiates a T cell response?
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Helper finds the complementary CD8 cell to make many copies of itself. One set banked, another set is the effector set.
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Generation of clonal diversity
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process of developing "library" of B and T cells that can respond to any antigen that we encounter. Mainly occurs in childhood, but a bit later in life too.
We produce all of the B and T cells before we ever encounter the pathogen. |
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What happens to the Pre T in the Thymus
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Gets CD4 or CD8 surface marker and T cell receptor, which indicates cell specificity -- what antigen the T cell can fight.
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How is clonal diversity for T cells made? What is the problem with this?
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V J and C genes are randomly mixed up. Because it is random, it can sometimes make combinations that target our own auto reactive cells. And thus there is clonal deletion.
Don't need to know more than that |
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Where does clonal deletion happen?
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In epithelia just outside thymus. Represents all self antigens in the body. This way, if a new T happens to bind to the self antigen on its way out, it is a signal for the thymus to destroy that T cell
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Central tolerance
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We tolerate ourselves. We do not makes cells that target ourselves. Central = happens in central lymph nodes and thymus gland.
Almost identical with B cells |
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What part of the brain helps trigger inflammation? What else in the body?
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Hypothalamus, liver and bone marrow are targets for systemic inflammation
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What are the cytokines names? What is their ultimate goal?
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IL1 IL6 and TNF Alpha
To make sure an immune response is triggered via systemic inflammation |
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What do cytokines act on? What does it do?
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Liver: increase production of acute phase response proteins (CRP and NBL) to increase complement activation
Brain: hypothalamus to make general malaise and increase body temperature Bone marrow : scavenger cells, monocytes to increase phagocytosis Fat: energy metabolism Dendritic cells: TNF makes them go back to the lymph nodes to make sure a proper response is happening |
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What is another name for maladaptive systemic inflammation?
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Sepsis
When an infection is in a tissue, systemic inflammation is moderate and adaptive. If the infection gets into the bloodstream, triggers sepsis. Greatly exaggerated response that is fatal Cytokines also dump reactive oxygen species systemically, which isn't good. Causes drop in blood pressure and septic shock. |
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Why is septic shock dangerous?
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Less blood flow to all of our organs from drop in BP
Disseminated intravascular coagulation -- paradoxical hemmorage, causing overactivation of clotting cascade |
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Are viruses in ICF?
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No -- they live in the cells. Host cell has to present
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How does the host cell know that it is infected?
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It detects double stranded RNA inside itself -- humans don't do that
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What 3 things does a host cell do when it detects a virus in it? What does it release to notify these procedures to initiate?
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Releases cytokines interferon Alpha and Beta to affect host and neighboring cells to:
1) Host cell and neighboring cells to make enzymes to break down RNA 2) MHC1 production increased 3) activate NK cells in innate immune system to release interferon gamma to potentiate alpha and beta as well as destroying the host cells |
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Complete resolution
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After healing, the tissue looks and functions exactly the same as it did before the damage
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Puss stage resolution
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formation of an abscess. Happens with infection of certain bacteria that are difficult to clear. Causes perpetual attraction of neutraphils, which die upon arrival and create the puss.
Puss = collection of neutrophils. Usually leads to scarring |
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Scar tissue resolution
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Happens when tissue cannot regenerate the same cells
Happens with myocardial infarction--heart cells cannot replicate. Healing occurs through fibrotic scar tissue remodeling, which is not as functional |
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Chronic inflammation resolution and causes
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An injury that is not acute--persistent.
Conflicting events of active inflammation and events to repair tissue. Frustrated repair if chronic inflammation is not interrupted, will make scar tissue Syphilis does this. Hepatitis. Chronic hyperglycemia and cholesterol. Alcohol Exogenous or endogenous |
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What happens after neutrophils release reactive O2 and die?
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Monocytes come and turn into macrophages, cleaning up the mess. Continue inflammatory mediators but also clean up. Phagocytose neutrophils and dead pathogens, escaped proteins.
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Early vs late macrophages
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Early in damage: stimulating inflammation and cleaning, leave the tissue
Later in healing: release anti inflammatory cytokines and growth factors for tissue and blood vessels and then leave the tissue |
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frustrated repair
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Attempts to repair tissue by cytokines but the ongoing inflammation from other cytokines damages the attempts to repair. Happens in chronic inflammation. Debris and cells can't leave tissue/constantly recruited to the area. Macrophages release pro inflammatory and pro healing.
As a result, only fibrotic scar tissue survives. Loss of function |
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Purposes (3) of the complement system
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Promotes inflammation
direct killing opsonization/tagging, to increase phagocytosis |
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How is complement activated? (3)
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Presence of a pathogen
part of systemic response, the liver Adaptive immune system via antibodies VIA CLASSICAL, MBLECTIN OR ALTERNATIVE |
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Classical pathway to complement system
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C1 starts the cascade (binds to pathogen surface, binds to c reactive protein produced by liver in systemic inflammation, C1 binds to pathogen antibody)
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MBLectin pathway to complement system
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MBL, produced in liver during inflammation, acts like C1 -- increases probability of complement action. Binds to pathogen surface and that binds to the second complement and triggers cascade.
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Alternative pathway to complement system
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Inactive C3 binds to pathogen surface
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Outcomes of complement
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Promotes inflammation
Opsonization Membrane attack complex (tunnel made from complement protein inserted into pathogen cell wall) |
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4 Outcomes of Kinin system
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Bradykinin promotes localized vasodilation/cap permeability, enhancing vascular effect of inflammation
Activates pain receptors to make inflammation painful Chemotaxins for neutrophils Stimulates complement system |
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The enzyme that activates the kinin system also activates what?
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Factor 12 clotting system, which results from blood vessel damage.
When neutrophils arrive at inflammation site, they release this factor to start kinin system. |
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What are the two ways the clotting cascade is triggered?
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Damage to the blood vessel surface, releasing activating 12
Damage to the tissue outside of the vessel, producing mediator tissue factor and activates further down the cascade at 10 |
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What is the outcome of the clotting cascade? What is the key step
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a clot.
Prothrombin, precurser, turns into active thrombin. Thrombin is the key enzyme that makes the clot, converting fibrinogen into fibrin, which cross link and makes a net for RBCs |
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First thing that happens in an adaptive immune response?
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After clonal diversity, antigen presenting
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Antigen Presenting Cells (3)
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Dendritic cells
Macrophages RARELY Mature but naive B lymphocytes, while making migration. |
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How is the dendritic cell best for antigen presenting?
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It is the only antigen presenting cell whose sole purpose is presenting
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What do B cells mainly respond to?
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Extracellular bacteria/fungi/paracites like (pneumonia tetanus sleeping sickness)
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What do adaptive T cell responses tend to target?
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Intracellular infections (malaria, leprosy)
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Cell mediated immunity
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T cell responses. What you are getting to act and fight are affecter cells. TH1
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Antibody mediated immunity
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B cell responses are also called, TH2
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What do intracellular infections tend to infect?
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Macrophages after phagocytosis. Bacteria shut down the process of breaking them down.
TH1 has to come along, sees the antigen on the surface of the macrophage, and fuses lysozymes and bacterial pockets |
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Interleukin 2 4 5 6
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Released from CD4 cell after macrophage presents via MHC2 to CD4 T cell onto CD8 cell and causes cell division and proliferation
a set of memory and a set of effector cells are created |
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neutralization
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Antibody attaches to pathogen and blocks replication/infection of cells
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Effects of complement
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inflammation, Neutralization, opsonization membrane attack complex
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IgG
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Monomer, tags for opsonization and neutralization
Sticks around for the next time exposed to antigens ready to neutralize. Number doesn't go down as much |
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IgM
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Activates Complement
Forms B cell receptor with IgD First wave of antibodies produced after initial infection, but returns. Initial inflammation PENTAMER, ten binding sites, what it lacks in affinity it makes up for in avidity (number of sites, greater chance to connect |
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IgA
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Neutralization
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IgE
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Sensitization of Mast Cells and allergic reactions
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IgD
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Forms B cell receptor with IgM
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Class switching
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Varies attack for a single pathogen to be more effective
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Affinity Maturation
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How tightly the bind between antigen and binding site.
Initial exposure has low affinity binding with antigen. The waves of IgG has a higher affinity and all of the antigens in the second infection are highest. Given more experience, we produce antibodies of higher affinity |
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Vaccine
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initiates antigen in the system without the pathogen. Need boosters, though, because antibody titers get low and you won't have immediate protection. Time is key
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Allergy
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Immune response to a non harmful environmental antigen
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Alloimmunity
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Reacting to someone else's self antigen
Usually T Cell mediated 4 |
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Type 1 - immediate hypersensitivity
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Anaphylaxis -- true allergies
Mast Cell Sensitization - We are producing IgE to sensitize Mast cells--degranulate and cause inflammation. IL1 also does this |
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Type 2 -- antibody mediated hypersensitivity
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Looks appropriate -- has the IgM and IgG
Often autoimmune, anemia, tags and kills RBCs Same as any antibody mediated response except against non harmful antigen |
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Type 3 -- immune complex mediated
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Antibodies attached to chunks of destroyed pathogens get stuck in tissue -- such as capillary filter in kidneys.
When this gets stuck, triggers complement and inflammation, damaging tissue. |
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Type 4 - cell mediated hypersensitivity
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Antigen activation of T cells, which causes direct killing and inflammation
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hyperacute rejection/humoral
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Very fast -- before patient gets off the table. Alloimmunity already exists
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Acute rejection
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most common form of rejection. within 6 months
t cell response on cells in organ, antibodies on blood vessels in organ usually t cell mediated |
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chronic rejection
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harder to control -- organ just diminishes in function over time
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GVH
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Graft vs Host
immune competent cells in immune compromised person. Donor attacks recipient. Acute or chronic |