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| Question | Answer |
| What is the purpose of inflammation in immunology? | To induce vasodilation to allow immune cells and cytokines to easily get to the site of infection |
| What are the cardinal signs of inflammation? | Calor - Heat Oedema - Swelling Rubor/Erythema - Redness Dolor - Pain |
| What specifically triggers the immune response? | PAMPS and DAMPS (danger associated molecular patterns) (pathogen associated molecular patterns) |
| Name the groups of chemicals that act as mediators of inflammation | Cytokines Auxiliary Cell Mediators Anaphylatoxins |
| State the cytokines involved in inflammation | TNF - A IL-1b IL-6 IL-8 |
| State the auxiliary cell mediators involved in inflammation | Histamine, Prostaglandin, leukotreines |
| State the anaphylatoxins involved in inflammation | C3a C5a |
| Outline the process of leukocytes moving out of blood vessels | 1 - Blood vessel wall is activated -Endothelial cells increase adhesin expression -Leukocyte intergrins bind to endothelial cells -Cells roll along vessel wall and tether and adhere 2 - Tight junctions between cells become permeable -vasoactive amines increase vessel permeability (histamine) -cells squeeze between endothelial cells via diapedesis 3. Cells extravasate into the tissues |
| How would you summarise innate immunity? | General, non-specific, constantly there, defence |
| State the properties of innate immunity | Non-specific to antigen - broad spectrum Fast acting Provides no memory to antigen 1st line of defence |
| Give examples of external barrier that make up the immune system | Skin, mucous, cillia, enzymes, pH, commensal organisms |
| How do commensal organisms perform their innate immunity function? | They compete for space and nutrients against pathogens |
| How does lung surfactant carry out its innate immunity function? | It is an antimicrobial liquid |
| In terms of immunity, what is chemotaxis? | The process of attracting and moving cells to an area |
| Define Opsonisation | The process of coating a pathogen in opsonin to increase its affinity for phagocytes |
| What do mast cells release? | Histamine, leukotrienes, prostaglandin |
| What do platelets secrete? | Serotonin |
| Define cytokines | Chemical Messengers |
| Run through the list of interleukins | Back of inflammation handout out or http://thjuland.tripod.com/interleukin.html |
| What are acute phase proteins? | Liver derived proteins which assist the complement system and also produces opsonins. Also produces clotting factors as the immune response may be due to a break in the skin |
| Name two cytotoxic cells involved in the non-specific response | NK Cells Eosinophils |
| What are the ways in which a phagocyte can bind to a pathogen? | Directly via antigens Via complement (opsonisation) PAMPS |
| What are the two ways in which phagocytes can kill? Give some examples | O2 dependent - toxic 02 derived products -Toxic NO's O2 Independent - Anti - Microbial peptides - Enzymes -Acidification |
| What are PAMPs and how do they work? | Pathogen Associated Molecular patterns - These are components of the pathogen, not necessarily antigens, which can directly activate B-Cells. The PAMPs which can directly activate B-cells is known as T- Independent Antigens, as T-cells are not required to activate the B-cells |
| What are the functions of antibodies? | -Neutralise toxins -Neutralise pathogens -Block pathogen receptors -Activate complement -Attract T-cells to kill the pathogen |
| What are the 4 ways in which a phagocyte can bind to a pathogen? | Increasing in strength: 1. Phagocyte binds to pathogen via non-specific cells 2. Phagocyte binds using antibody 3. Phagocyte binds using C3b 4. Phagocyte binds using C3b and antibody |
| What is cytokine storm? | Hypercytokinemia - The overproduction of cytokines caused by a break in the feedback loop. The continued production of leukocytes leads to continued cytokine production and eventually it can lead to septic shock |
| Describe and outline the structure of an antibody | -Consists of heavy and light chain -Joined together by disulphide bonds - The heavy chains at the bottom are known as constant/Fc region - The light chains are known as variable/Fab regions -The heavy chains run along the inside all the way to the top, whilst the light chains are only on the outside portion of the top |
| What determines the class of the antibody? | The type of heavy chain |
| Describe the structure of IgA | Dimer consisting of 2 antibodies joined together by a J chain with a central secretory region |
| Describe the structure of IgM | 5 antibodies joined to forms a pentamer with a J chain |
| Which of the antibodies are monomers? | IgG, IgE and IgD |
| Define Antibody Isotype | The class of antibody. Eg. IgA, IgD etc. |
| Define Antibody Allotype | Genetic make up that forms an individuals structural make up of the constant region/ heavy chains |
| Define Antibody Idiotype | The structure of the variable/ FAB region |
| How do immune cells bind to antibody? | The antibody binds to the pathogen using the variable region and this activates the Fc region, where phagocytes, mast cells and NK cells can bind to. Mast cells specifically have receptors for IgE molecules |
| Describe the process of microbe defence in secretions such as mucous, tears and saliva | IgA binds to microbe an neutralises it The microbe gets trapped in the mucous Mucous is removed or swallowed if in the throat. |
| How many antigen binding sites does IgM have and why does this not happen in reality? | It has 10 binding sites but due to the close proximity, there is usually not enough room to bind antigens next to each other |
| Which is the first antibody produced in the immune response? | IgM |
| When and what is the second antibody produced? | IgG is usually second, but only after class switching which occurs in the secondary response. |
| Which antibody is found in mucosal secretions? | IgA |
| What does IgE do and how does it work? | It binds to mast cells and acts as a receptor to fight parasites and worms |
| Which is the only antibody that can protect the foetus by crossing the placenta? | IgG |
| Define Antibody Affinity | How strongly an antibody will bind to an antigen |
| Define antibody avidity | How many potential antigens the antibody can bind to. Eg. IgM has the highest avidity |
| What are immune complexes? | The complex formed when antibody and antigen bind. A single antibody-antigen complex is a single immune complex, however this immune complex can bind to several other immune complex, hence forming large immune complexes as seen in pictures. |
| What does the formation of an immune complex do? | Activate complement. |
| Which complement protein works to make immune complexes more soluble so that they are more easily removed? | C3b |
| Describe the process of transporting immune complexes | When the complement protein C3b binds to the immune complex it is then able to bind to the CR1 receptor found on red blood cells. The red blood cell transports the immune complex to the liver. In the liver, the Kuppfer cells also contain CR1 receptors which can bind to the immune complex. The kuppfer cells bind to the immune complex via the receptors which are not in use by the red blood cell and they pull the immune complex off the red blood cell. The kuppfer cell then takes up the complex and destroy it via phagocytosis. |
| Describe how an immune complex will struggle to be cleared and what the consequences are | The inability to clear immune complexes leads to a Type 3 Hypersensitivity attack. It occurs via the following process: -Immune complexes fail to activate complement (usually small ones, hence why large ones form) -Hence they are not picked up and travel around the body and are deposited -They are mainly deposited in blood vessels, joints and glomeruli. -The deposition continues until the accumulation is so large, complement is activated -The process of complement, with inflammation and leukocytes arriving and attacking the stuck immune complex will cause damage to the surrounding tissue -In the kidney, the inflammation and tissue damage can lead to kidney disorders -One phenomenon that occurs is frustrated phagocytosis, where the phagocyte attempts to engulf the complex, but because a section is stuck in the tissue, it cannot get all the way around. It ends up releasing its cytotoxic enzymes anyway, which leads to spillage and further tissue damage. |
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