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71 Cards in this Set
- Front
- Back
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What are the 4 types of hypersensitivity? |
1. Type I: Immediate hypersensitivity --> IgE 2. Type II: Cytotoxic hypersensitivity --> IgG or IgM 3. Type III: Immune Complex-mediated reaction --> IgG 4. CMI (cell - mediated immune receptors) --> delayed response. |
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Describe the phases of Type I hypersensitivity |
Phase I: Sensitization - production of IgE Phase II: Activation of degranulation Phase III: Effector Phase IV: Late Reaction |
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Which types are cell mediated and which types are antibody mediated? |
antibody mediated: Type I, II, III Cell body mediated: Type IV |
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Effector function of Th cells in a HEALTHY person: |
Balance between Th1 and Th2 Th1 produces igG (neutralizes the reaction) |
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Effector function of Th cells in a SENSITIZED person: |
Th2 is stronger and release igE (reaginic reaction) |
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What occurs with activated mast cells? |
activated mast cells will release IL-4 and this will stimulate the plasma cell to release IgE. |
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What occurs when IL4 is released by mast cells? |
IL4 will result in the switch from igG to igE --> hypersensitivity reaction. |
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What are the 3 mechanisms in Type II Hypersensitivity? |
1. Complement mediated reaction: interaction between a specific antigen and the antigen on the cell membrane leading to lysis or phagocytosis. 2. ADCC: cells expressing the Fc receptor 3. Antibody mediated dysfunction: the receptor on the target antibody is blocked leading to impaired cell function. |
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Explain Rh - and + in 1st and 2nd pregnancy |
1st pregnancy: mom is Rh - and baby is Rh +, mom develops an anti Rh (IgM) which does nto cross the placenta 2nd pregnancy: the anti Rh is turned into IgG and can cross the placenta and attack the babies RBC --> hemolytic anemia. |
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What is the fate of an antibody? |
1. phagocytosis 2. removal by erythrocytes (elimination in the liver) |
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Type III: local immune complex-mediated reaction *COMPLEMENT ACTIVATION |
1. locally injected antigen (IgG) 2. complement system activated 3. binding of immune complex to FC --> degranulation occurs 4. inflammation, increased fluid, protein, phagocytosis. |
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What is serum sickness? and when does it occur? |
when someone is injected with protein for therapeutic reasons and there is an overproduction of pro-inflammatory protein and may occur in arthritic pts. occurs when the complement drops too low *basically when ppl receive protein their complement system is heavily monitored. |
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Mechanism of type IV hypersensitivity reaction |
Stage 1: sensitization - activation and processing of antigen by APC Stage 2: Delayed response initiated due to repeated exposure. get a release of cytokines and accumulating T cells. This reaction uses Th1 response*** |
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What activates the complement system? |
1. Antigen- Antibody complex 2. CRP and MBL |
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What are these T cell dependant responses wiith respect to their protein antigens? IL4 IL2 IFN TGF |
IL4 - IgE IL2 - IgM IFN - IgG TGF - IgA. |
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What corresponds with humoral immunity? |
Aquired immunity. |
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Type I hypersensitivity |
- IgE - immediate response - anaphylactic - attaches to mast cells, basophils and parasites--> degrranualtion --> releases histamines |
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Type II hypersensitivity |
- IgG or IgM - Cytotoxic/ cytolytic - IgM (primary antibody), IgG (secondary) - example: BLOOD TYPE (type II) |
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Type III hypersensitivity |
- IgG - immune complex --> antigen binds to anibody and activates the compliment system (C5a binds to C5a receptor on mast cell --> degranulation) - vasculitis can occur, rheumatoid arthritis - Systemic and Soluble |
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Type IV hypersensitivity |
DELAYED TYPE HYPER. (DTH) - repeated exposure to antigen --> gets worse - deals with T- cells NOT antibodies (cell mediated) - cytokines dictate the T cell response |
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which products are pro - inflammatory that are released by Th1? |
IL2 and IFN (TNF is pro-inflammatory as well) |
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which products are anti-inflammatory that are released by Th2? |
IL4 and IL5 |
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What 4 specific products do mast cells produce? |
1. prostoglandins 2. leukotrienes 3. cytokines 4. histamine |
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Steps of type 1 hypersensitivity. |
1. sensitization - allergen present, Th2 increases --> releases IL4, IL5, class switch from IgG --> IgE 2. Second exposure --> memory B cells activated --> Plasma cells --> mast cell activation --> increase in IL4 and IgE 3. Histamine 4. Effects of degranulation products |
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what occurs in antibody mediated cellular dysfunction? |
autoantibodies block the fc receptors on target cells to decrease phagocytic function. example: myasthenia gravis |
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Antibody dependant cell mediated cytotoxicity (ADCC) process |
antibody binds to antigen, NK cell recognizes it and kills it. |
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what occurs in a complement mediated rx? |
Antibody binds to antigen and forms the MAC complex --> opsonization and lysis. |
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what is the difference between type II and type III hypersensitivity? |
type II - In tissues, Cell - associated type III - Soluble, Systemic circulation |
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What occurs in Type IV hypersensitivty? |
Delayed - presentation of antigen by APC --> Th1 activated and releases IL2, IFN and TNF which lead to macrophage activation. example: TB test, jewellery (IL2 - increases # of T cells) (IFN - increases macrophages and dendritic cells) |
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HistoCOMPATIBLE relationships: |
Autograft (skin from thigh to arm) Syngenic (genetically identical - kidney from one identical twin to the other) |
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HistoINCOMPATIBLE relationships: |
1. Autologous - genitically diff (fraternal twins) 2. Xenologic - diff species (liver from a pig) |
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MHC class I |
presents a foreign body to cytoxoic Tcells if they lack MHC receptr -> activates NK cells and kills cell. ENDOgenous/ INTRAcellular CD8 |
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MHC class II |
present on APC cells and dendritic cells EXOgenous reaction CD4 (T HELPER cells) |
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What occurs in organ transplant rejection? |
the host attacks the organs |
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what occurs in bone marrow transplant rejection? |
the T cells attack the host |
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What happens in Graft vs. Host disease? (GVHD) |
Donor T cells are sensitive to host MHC and attack epithelium. |
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T cell independant reaction and babies |
babies have low IgM - cannot respond to T cell independant rxn - T cell independant can activate B cells without a T cell and produce ONLY IgM. |
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what is immunoscenesense? |
remodelling the immune cells via shortening of telomeres. |
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what happens in immunosenesense and innate immunity? |
altered intracellular pathways like phagocytosis - cells can be phagocytosed but NOT killed. |
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what happens in immunosenecense and adaptive immunity? |
anergy (decreased reaction) in co-stimulatory molecules |
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what occurs in a precipitation reaction? |
soluble reaction - lattice forms ina zone of equivalence between antigen and antibody if too much antibody --> not enough antigen to bind and vice versa. |
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what occurs in an aggluttination reaction? |
tests for BACTERIAL binding NOT antigenic - IgM antibody is used because of its many binding sites - bacteria is cultured with dye bound anti-bacteria antibody and then clumps - if no anti-bacteria antibody present, but bacteria is --> no clumping. |
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coombs test is used when? |
for antigen detection and in aggluttination - used to determine Rh factor in baby and mother |
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ELISA is used when |
enzyme linked immunosorbent assay in precipitation rxn - used to determine concentration of CK receptors - like IL1 |
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RIA (radioimmunoassay) |
- used for small compounds like hormones (hot and cold antibody - isotopes/ no isotopes) |
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western blot souther blot northern blot |
western blot - protein analysis southern blot - specific DNA analysis northern blot - RNA analysis |
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what does Treg release? |
TGF and IL10 |
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products of tumour cells can suppress what? |
TGF beta (function is apoptosis, control cell differentiation and proliferation) |
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Innate immunity |
- present at birth - NK cells, macrophages, cytokines - non- specific NO MEMORY |
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IL 12 cytokine: |
Th1 promoting cytokine Th1 --> IFN and IL2 (pro-inflammatory) |
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what is the biologic action of TNF |
bone loss |
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What occurs in Type I hypersensitivity response? |
You inhale an allergen and this allergen goes to lungs for example, a macrophage will come and engulf it. Th2 will release IL4 and B cells will mature into Plasma cells. Class switching from IgG to IgE occurs and IgE binds to the mast cell. The allergen then binds to IgE on the mast cell and degranulation occurs --> Histamine, PG, cytokines --> INFLAMMATION. *Mast cells make the vessel more permeable for things to go in. |
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How do antigens present themselves in Type II hypersensitivity? |
1. soluble: antigen floating in blood, antibody binds and activates complement system. (C3b engulfs) 2. cell bound (good pasters, farmers lung, haemolytic anemia) 3. receptor mediated (myasthenia gravis) |
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What are some examples of reactions occuring in Type II? |
Blood transfusion reaction Goodpastures |
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What are the products activated in the complement system? |
C3a andC5a - activate macrophages and neutrophils C3b - opsonization C5b - initiates MAC complex |
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What are some examples of reactions occurring in Type III? |
Rheumatoid Arthritis SLE - Lupus Vasculitis |
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What occurs in Type IV hypersensitivity? |
Delayed response with repeated exposure to an antigen it will be engulfed and a macrophage/ dendritic cell(MHCI or MHCII) will present to the T cell (either Thelper or Tkiller) and will produce the respective one. |
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Allergic patients will have reduced activity of ______ cells |
reduced Th1 cells |
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Activated _____ cells will produce IL4 and lead to ____ production by plasma cells. |
Activated MAST CELLS will produce IL4 and lead to IGE production by plasma cells. |
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What are products of the arachidonic acid cascade? |
Cox (Cyclooxygenase) --> prostoglandins Lox (Lipoxygenase) --> leukotrienes. |
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What is Cyclosporin? |
- most affective immunosuppresor - very little IL2 is produced - produces TGF beta |
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What are attenuated viruses? |
when a pathogen is taken from a human and is put into a monkey for example and it then undergoes mutations and changes and will not be affective in a human so it is then used as a vaccine. it is made in temperatures < 35 degrees. |
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Function of Tregs? |
Down regulates allergic responses. |
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Function of Vitamin A? |
produces IgA helps to regulate Th1 and Th2 balance via differentiation of Tregs. |
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Function of Vitamin D? |
increases activity of Tregs DECREASES Th1 response Can help with treating autoimmune disorders *stimulates innate immunity *inhibits adaptive immunity |
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The principle mechanisms in Aquired immune mechanisms against EXTRAcellular pathogens |
Humoral immunty |
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The principle mechanisms in Acquired immune mechanisms against INTRAcellular pathogens |
Cellular immunity |
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Babies 0 - 24 months cannot develop an immune response to ___________ response? |
T cell independant* so they get conjugate vaccines with polysaccharides. |
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T independant cell function? |
Produce ONLY IgM Leave NO MEMORY Do not induce cytokines production. |
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In babies what is reduced in the immune system? |
reduced complement system reduced Th1 Increased Th2 Tregs are strong. |
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Which cytokine induces bone loss (increases osteoclast activity)? |
TNF |
