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62 Cards in this Set
- Front
- Back
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What disease can have a vaccine used for treatment after infection?
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Rabies
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What is bad about passive immunization?
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Passive immunization gives only temporary immunization and there is no memory response
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Where is passive immunization seen?
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The maternal IgG for fetus, it used in immunodeficiency, emergency protection against know exposure, mile IgA for newborn.
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What are the disadvantages and advantages in inactivated antigen vaccination?
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The advantages are it is:
It is very safe, no chance of reversion or mutation. It will have a strong shelflife. Will give a strong hummoral immunity if enough antigen present. The disadvantages are: have to give booster shots to patients. They may fail to inactive the vaccine There is no CTL response because this a exogenous pathway There will be primarily Th2 instead of Th1 There will be few IgA |
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What are the disadvantages and advantages of live antigen vaccines?
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Advantage:
Will activate all phases of immunity. Will acquire immunity quickly Will go from Th1 to Th2 Can be administered easily Will have IgA and IgG Disadvantages Vaccinee may become contagious. Virus could revert to virulent form Hard to store |
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What are two cases were the vaccination will give worse symptoms?
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GBS and Atypical measles
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Is vaccination ever given via IV?
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NO!!! It is always given via subcutaneous (muscle)
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What are three adjuvants that were described in clas?
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MF59, Freund's adjuvant, aluminum hydrate.
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Plasmids are made to release to certain cytokines to give an immune response?
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IFN gamma to give TH1
IL-10 to give TH2 |
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How are allergens, Th2, and IgE related?
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Allergens will invoke response of cytokines, (IL-4 and IL-10)
These cytokines will promote production of IgE |
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What will happen when an antigen binds to IgE, relating to mast and basophil cells?
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The bound IgE will then bind to mast cells and basophils and will cause degranulation of active chemicals (histamine)
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What antibody (Ig) will be seen in a unusually high percentage with subjects with type 1 hypersensitivity?
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IgE
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Besides histamine and Arachadonic acid, what else is released and what mediates this release in mast cells?
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A signal cascade response mediates the degranulation and leukotrienes are released which will play a factor in bronchoconstriction .
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What will inhibit the type 1 hypersensitivity?
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IFN-gamma will inhibit Th1
A large amount of antigen will cause a switch from IgE to IgG |
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What are some therapies of type sensitivity?
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Inject large amounts of antigen and will cause IgE switching to IgG
Take anti-histamines Take EPINEPHRINE- which will cause vasoconstrion Take steroidal anti-inflammatory cortisone, this will relieve pain |
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What is the function of complement?
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Lysis of cells
Promote opsonization Clearance of immune complexes in spleen and liver Interaction with complement receptors |
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Where are complement molecules made primarily and secondanly
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Primarily made in liver but also made in monocytes, macrophages and epithelial cells of the GI tract
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What is thee purpose of C3 Convertase
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Enzyme which cleaves C3 into C3a and C3b. The small letter is in recognition of the proteolytic fragment.
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What can complement activation result in production of?
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Opsonins, Membrane Attack Complex and Inflamation and Chemoattractants
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Describe the classical pathway initiation?
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First antigen binds to antibody
This binding causes a change in Fc region of constant region Constant region will then bind C1 C1 is now activated and will serve as a serine protease for C2 and C4 |
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Describe the process in the classical pathway for complement following activation?
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C4 and C2 have now been cleaved by C1.
C4b will then bind near C1. C2b binds near C4b forming the C4b2b complex. This complex is called C3 convertase and it will cleave C3 into C3a and C3b. The cascade will continue through cleavage of C5 forming the Membrane Attack Complex. |
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Describe the alternative pathway
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The C3 will undergo slow hydrolysis and form C3a and C3b.
C3b gives a positive feed back loop and makes more C3b C3b will bind to membrane components, foreign and host C3b with binding of other proteins will form C3 convertase |
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Describe the lectin pathway in complement?
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The MBL will of course bind Mannose.
The MBL will then bind to MASP and form a complex similar to C1. The MBL-MASP will then cleave both C2 and C4 |
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What complement factors make up the Membrane Attack Complex And what is the function of C9?
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C5b, C6, C7, C8, C9
C9 will cause a large pore in target cell membrane, which allows free diffusion of small molecules through the membrane(death) |
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What is able to avoid attack from the MAC?
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Gram positive bacteria due to thick cell walls
Capsules may also prevent lysis |
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What complement factors will cause degranulation in mast cells and basophils, they are called anaphylotoxins?
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C3a, C4a, C5a
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What complement factors are strong chemoattractants for neutrophils and monocytes?
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C3a and C5a
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What is does the complement receptor 1 (CR1) do when bound to C3b and where is CR1 usually found?
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It is found on many different cells, including monocytes and neutrophils.
It is a powerful inducer of phagocytosis for neutrophils |
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The activation of Tdth will cause the release of which cytokines?
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IL-2, IFN-gamma, TNT-beta, and the macrophage inhibition factor
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When the Tdth is activated in Type 4 hypersensitivity what will occur?
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Macrophages will go to site and relase lytic enzymes
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What can Type 3 Hypersensitivity cause?
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Neutrophil activation and inflammation
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What are the classic signs for inflammation?
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Redness
Warmth Pain Swelling |
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When an tissue is injured the tissue will release chemicals such as what to nearby capillaries/endothelial cells?
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Selectins-These are cell adhesion molecules.
The WBC's adhere to selectins. The neutrophils (WBC) will then express integrins |
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When there is tissue injury there is a decrease in pH which activates what?
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Kallikreein
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What is the function of Kallikrein? Also what is the function of bradykinin?
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Kallekrein cleaves bradykinin to release active bradykinnin peptides.
Bradykinin opens junction between endothelial cells allowing greater access to more leukocytes and fluid from blood, binds to mast cells relasing histamine (vasodialator) and heparin (anticoagulant). |
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Besides the kallikrein and selectins, what else is released in acute inflammation?
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Nerve cells release sub P (vasodilator and stimulates pain perception)
Arachidonic acid is released from many cells and metabolized into prostaglandins (vasodialator and prostaglandins) |
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Why is vasodialation imp in tissue injury?
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This allows for permeability in capillaries, allowing flud from blood to accumulate at site of injury
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What are some of the causes for chronic inflammation?
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Persistent infections and autoimmune disorders
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What is a granulomas?
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Macrophages that surround a pathogen. Happens when a persistent infection and phagocytes can't clear the pathogen.
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What mycobacterium causes formation of granulomas?
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Myocbacterium tuberculae
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The relase of inflammatory signals from dead cells will bind to TLR's and cause the release of what and this causes what?
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Cytokines and this causes vasodialation
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Describe what happens with IgE, basophils, mast cells, IL-4 and IL-10.
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IgE will bind to mast cells and basophils and then when it encounters antigen.
The mast cells and basophills and will degranulates releasing histamine which will bring: Vasodilation Smooth muscle contraction (but not blood cells), bronchoconstriction |
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What is atopy?
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This is an abnormal amount of IgE in the absence of a parasite.
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When mast cells, which are located near connective tissue degranulate, they release numerous chemicals like....
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Histamines – there are three histamine receptors, H1, H2 and H3. H1 mediates most effects, including bronchoconstriction, mucus secretion, vasodilation and increased vasopermeability.
Arachadonic acid is produced and then converted into Prostaglandins (inflammation, pain). NSAIDs inhibit the enzymes which mediate this process. Leukotrienes (bronchoconstriction, mucus secretion) are also produced, and can cause bronchconstriction and mucus secretion. Singulair is a recently developed drug that blocks some leukotriene receptors. Other chemicals too |
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IL-4 causes switching to what IgE and IgG
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Diarheea
Asthma |
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What is atopy?
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This is an abnormal amount of IgE in the absence of a parasite.
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When mast cells, which are located near connective tissue degranulate, they release numerous chemicals like....
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Histamines – there are three histamine receptors, H1, H2 and H3. H1 mediates most effects, including bronchoconstriction, mucus secretion, vasodilation and increased vasopermeability.
Arachadonic acid is produced and then converted into Prostaglandins (inflammation, pain). NSAIDs inhibit the enzymes which mediate this process. Leukotrienes (bronchoconstriction, mucus secretion) are also produced, and can cause bronchconstriction and mucus secretion. Singulair is a recently developed drug that blocks some leukotriene receptors. Other chemicals too |
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IL-4 causes switching to what
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IgE and IgG
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Mast cells in these locations cause:
GI Tract Respiratory |
Diarheea
Asthma |
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Repeated antigen in body causes what?
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induce switch to IgG response or simply cause enough IgG production to out compete IgE for binding to antigen
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What happens in type II hypersensitivity?
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type II hypersensitivity is called antibody-dependent cell-mediated cytotoxicity (ADCC). Here, cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM). These tagged cells are then recognised by natural killer (NK) cells and macrophages (recognised via IgG bound (via the Fc region) to the effector cell surface receptor, CD16 (FcγRIII)), which in turn kill these tagged cells.
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What is the therapy used in type I hypersensitiy?
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Epi
Anti-Histamine Cortisone and other anti-inflammatories |
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Describe type III hypersensitvity?
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When antibodies bind to antigens, immune complexes are formed. Usually, they are cleared by phagocytosis but too much can cause tissue damage
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How does damage of type III happen?
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Damage may be caused by a number of factors, including release of lytic enzymes by neutrophils recognizing C3b.
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What happens in type 4 hypersensitivity?
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The Tdth will bind antigen and then secrete IFN gamma and IL-2, macrophage inhibition factor, and TNF-β.
This cause infiltration and activation of macrophages and release of lytic enzymes. Reactions take 48-72 hours to develop. |
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What are some of the functions of complex?
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Lysis of cells, bacteria, viruses
Opsonization Interaction of complement receptors, resulting in immune activation Immune clearance |
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Where are most complement molecules produced?
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Liver but also by monocytes, macrophages and epithelial cells of GI Tract
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The three pathways of complement lead to producing ?
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Convertase
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C3a is powerful chemoattrant and
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pro-inflammatory
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anaphylatoxins, these bind to receptors on mast cells and basophils and induce degranulation.What are anaphylatoxins?
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C3a, C4a and C5a
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C3a and C5a are also strong chemoattractants for ?
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neutrophils and monocytes
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CR1 is a powerful inducer of _____ for neutrophils and CR1 is a receptor for C3b.
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Phagocytosis
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