11352322
Description
Flashcards by Anna Hogarth, updated more than 1 year ago
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Created by Anna Hogarth
over 6 years ago
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| Question | Answer |
| What are the unconventional T cells? (3) | 1) yd cells 2) Intraepithelial lymphocytes 3) NKT cells |
| What happens to CD4 T cells with HIV/AIDs? | The virus only appears in the blood when CD4 T cell concentration drops below 200 cells/ul. For a long time it was not clear why the virus seemed not to replicated in the blood first - was later determined that the virus was being fought by CD4 T cells in the gut in Peyer's patches. |
| How does age relate to the onset of aids? | The younger the individual the faster the onset of aids |
| What receptor class presents to CD4 T cells? Where does this presentation take place? | 1) MHC class II 2) Lymph node |
| What is the receptor for IL-2? | CD25 |
| How does clonal expansion of T cells occur? | T cell recognises the correct peptide + MHC, autocrine secretion of IL-2 occurs |
| What are the 6 different effector CD4 T cells? | 1) Th1 2) Th2 3) Th9 4) Th17 5) Th22 6)Threg |
| Which cytokines are secreted by Th1 cells when activated? (2) | 1) IFN-y 2) TNFa |
| Which cytokines are secreted by Th2 cells when activated? (3) | 1) IL-4 2) IL-5 3) IL-13 |
| What is the primary function of TH1 cells? | Cell-mediated immunity |
| What is the primary function of Th2 cells? | Promote humoral immunity |
| Give two examples of mycobacteria | 1) Listeria 2) TB |
| How do Th1 cells interact with macrophages? | Secrete IFN-y which can activate macrophages containing mycobacterium (and virus) to help them kill the internal pathogen. |
| What are activated macrophages responsible for? | Scarring - foetal operations don't lead to scarring |
| What do Th1 cells do in response to TB? When is TB symptomatic? | 1) Walls off the infected cells - caseating granuloma. 2) Immune deficiency can results in dissemination of caseating granulomas resulting in the spread of TB and potentially the death of the individual |
| What do Th2 cells do? | Help B cells to make antibodies |
| How do B cells and T cells interact? | B cell can recognise the antigen via BCR in the lymph node (either freely or via antigen presenting cell). The BCR is then internalised via endocytosis and the protein is cleaved into a peptide. The peptide is then present on the MHC class II receptor and presented to the Th2 cell. If the Th2 cells has already encountered the antigen via an APC (DC) then the Th2 secretes cytokines (IL-4/IL-5/IL-13) to activate the B cell and trigger Ab production. |
| Which antibody class does IL-4 promote? | IgE |
| What do both Th1 and Th2 cells start as? | Th0 |
| Which cytokine is thought to promote the maturation of Th0 cells to Th2 cells? Which cell produces this? | IL-4 - secreted mast cells. Makes sense because mast cells respond to worms etc. and this then promotes the humoral branch of the adaptive immune system |
| What is responsible for redness etc. after the skin is scratched? | Prostaglandins secreted by mast cells |
| Which cytokines (2) are responsible for the maturation of Th0 to Th1? | IL-12 and IL-23 |
| In the context of the two branches of the adaptive immune system, what is thought to contribute to the increasing incidence of immune conditions? | Hygiene hypothesis - lack of exposure to allergens increases chance of developing allergies. No worms in the Western etc. therefore Th2 branch is free. |
| What are the two branches of leprosy? Which branches of the adaptive immune system are they mediated by? | 1) Tuberculoid leprosy - Th1 2) Lepromatous leprosy - Th2 |
| Which cytokines are secreted in tuberculoid leprosy? What does this activate? What is the prognosis? | 1) IFN-y 2) Activates macrophages, low number of organisms 3) Much more localised, treatable and survivable |
| Which cytokines are secreted in lepromatus leprosy? What does this activate? What is the prognosis? | 1) IL-4, IL-5, IL-13 2) Many antibodies produces - hyperglobulinemia, high number of organisms 3) This immune response is not good at controlling the disease, this results in disseminated disease which is much harder to treat with a much worse prognosis. |
| What are the two types of Leishmaniasis? Which branch of the adaptive immune response underlies each of these? | 1) Cutaneous leishmaniasis (orient boils) - Th1 2) Visceral leishmaniasis (black fever) - Th2 |
| Of the two branches of leishmaniasis, which has the worse prognosis? | Visceral leishmaniasis (disseminated version) |
| What are the two types of tuberculosis? Which branch of the adaptive immune response underlies each of these? | 1) Lepromatous TB - Th1 2) Miliary TB - Th2 |
| Of the two branches of tuberculosis, which has the worse prognosis? | Miliary TB is the disseminated version, it will spread to the spinal cord and brain. |
| What type of hypersensitivity is an atopic reaction? Nickel allergy? Eczema? | 1) Type 1 2) Type 4 3) Type 4 |
| Which cytokines are promote that maturation of Th0 to: 1) Th17 2) Treg | 1) TGFB, IL-6, IL-21 2) TGFB |
| What are the transcription factors expressed by the following: 1) Th1 2) Th2 3) Th17 4) Treg | 1) T-bet 2) GATA-3 3) RORyt 4) Foxp3 |
| What cytokines expressed by the following: 1) Th1 2) Th2 3) Th17 4) Treg | 1) TNF-a, IFN-y 2) IL-4, IL-5, IL-13 3) IL-17, IL-22 4) TGFB and other suppressve molecules |
| What roles the following: 1) Th1 2) Th2 3) Th17 4) Treg | 1) Defence against intracellular pathogens, promotion of cell-mediated immunity 2) Defence against extracellular pathogens, promotion of humoral immunity 3) Defence against extracellular bacteria (autoimmunity) 4) Immunosuppression (autoimmunity, cancer) |
| Where are T cells expressed in particularly high numbers, why is this? | In the gut - proteins in food induce the production of iT-reg cells which can then dampen down (switch of T cells) the immune system to prevent reactions to the food. |
| What is the function of immune memory cells? What are they essentially? | 1) Primed in order to induce a rapid immune response if the pathogen is re-encountered 2) Innate cells |
| Define immunological memory | The ability of the immune system to respond quicker and better to pathogens which have previously been encountered |
| When was the spanish flu? How many people died? What effect did this have on the number of deaths in the 1889 Russian flu outbreak? | 1) 1918 2) 50 million deaths (3% of the population) 3) Immunological memory protected the 40-75 age bracket |
| What is Rolf Zinkernagel's theory? When did he win a Nobel prize? | 1) Immunological memory does not exist - there is just a constant turnover of cells. If you beat an infection once, your immune system has shown that it is capable of beating the infection, why would you need to form a particular immunological memory? 2) 1918 |
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