Selkirk & Dionne - Immunology Flashcards
Definition of an antigen, B-cell receptor and T-cell receptor?
Antigen: Any molecule that is recognized by the immune system as foreign, specifically by lymphocyte receptors - can be any type of molecule protein, carbohydrate, lipid, etc.
B cell receptors: antibodies/immunoglobulins that are membrane bound or soluble –> immunoglobulins that are membrane bound are receptors but can also be secreted
T cell receptors (TCR): Receptors that are solely membrane bound
Why study the immune system? Why is it important?
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What are two major challenges facing people’s health related to the immune system?
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What are some examples of different types of vaccines?
Different types of vaccines developed to counter infection
- Whole organism - killed/inactivated (eg heat/formaldehyde)
- Whole organism - live attenuated (passage/genetic alteration)
- Subunit (purified product)
- DNA/RNA (encodes selected protein antigen)
Both Whole organism vaccines were initially used and quite effective
Have vaccines been succesful at treating/reducing disease incidence?
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What are the different physical barriers to infection? What are some examples of mechanical, chemical and microbiological methods employed by these barriers against infection?
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What is the innate immune system?
Innate immunity – Cells and components of the immune system which act without prior exposure to the pathogen
What is the complement system and what is it’s cascade?
Complement – a cascade of proteolytic enzymes which promote inflammation and cytotoxicity/
Apart from recruting effector cells, complement can form a membrane attack complex which inserts in the membrane of microorganisms to eliminate them - important for the initiation of immunity
Inflammation is another effect of activating complement
Cascade
- Presence of bacterial cell surfaces will induce cleavages and activation of complement fragments.
- One complement fragment binds to bacterium whereas the other acts as a chemo-attractor for effector cells
- Complement receptor binds to bacterium with bound complement fragment
- Effector cells perform phagocytosis - killing the bacteria cell + Chemo-attract fragment attracts further effectors
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What is inflammation? Outline the inflammatory response created when there is a cut in the skin
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What are cytokines and chemokines?
Cytokine: secreted protein which changes the behavior/response of neighboring cells think of them as short range hormones
Cytokines otherwise known as Interleukins (messages between leukocytes) – classified by numbers, e.g. IL-4, IL-5
Chemokine (specific cytokine) : Chemoattractant cytokine – attracts specific classes of cells
Differences between the innate and adaptive immune system?
Innate and adaptive immunity work in concert to control or eliminate pathogens
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What does this graph show? What can we takeaway?
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Red –> no immune response (infection grow exponentially)
Green –> Only innate immune system (intial response but lacks adaptive immunity to help clear pathogen)
Yellow –> innate and adaptive working properly
Primary (first) infection cleared by combination of innate and adaptive immunity
Innate immunity initiates first and is required to prime the adaptive immune response, whereas adaptive immunity required (generally) for pathogen clearance
Both are necessary and work together
What are the receptors expressed by macrophages called and what type of molecules do they recognize?
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What are Toll-like receptors?
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What is the adaptive immunity?
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Outline the general life cycle of B lymphocytes?
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What is Haematopoiesis and what organs are responsible for carry out this role?
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What is the composition of immune cells in the blood?
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What are NK cells?
NK cells - specific type of lymphocyte known as a natural killer cell – even though it is a lymphocyte it is part of the innate immune system
Outline the different lineages that a Haematopoietic stem cells gives rise to?
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Haematopoietic give rise to different lineages
a) Lymphoid Lineage
b) myeloid lineage
Lymphoid - Differentiation to B-cells (plasma or memory cells) or NK or T cells
Myeloid - includes White blood cells and red blood cells
a) Erythroid Progenitor gives rise to
- Erythrocyte – Red blood cells
Platelets - fragments of cells involved in blood clotting
b) Granulocyte-macrophage progenitor give rise to
- Mast cells
- Neutrophil, Eosinophil and basophil
- Macrophage and dendritic cell
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From a Haematopoietic stem cell, what determines the cell’s fate?
Lineage differentiation and development is controlled by transcription factors
Expression of these transcription factors is influenced by the environment - e.g. cytokines mediates the way in which the precursor cells differentiate
What are small lymphocytes, plasma cells, dendritic cells and mast cells?
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What are dendritic cells?
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What are the roles of NK cells, Neutrophils, Monocytes and Macrophages?
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Macrophages Visualization?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/747/694/a_image_thumb.png?1618405908)
What does opsonisation mean?
Opsonization is coating a pathogen with a molecule that facilitates its uptake, e.g. antibodies and complement
How do macrophages normally respond to the presence of pathogens (2 things)?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/747/900/a_image_thumb.png?1618406238)
Outline the role of Neutrophils in response to infection
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What are eosinphils, basophils, Megakaryocyte and Erythrocytes?
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What is the primary/central lymphoid tissue?
Primary (or central) lymphoid tissues - where lymphocytes develop (produced, mature and selected), this happens in…
Bone marrow - Naïve B-cells released by Bone marrow + T-cells start in bone marrow but move to the Thymus
Thymus – bi-lobed organ at the top of the chest - development of T-cells
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/748/352/a_image_thumb.jpg?1618406544)
What are the secondary/peripheral lymphoid tissues?
Secondary (or peripheral) lymphoid tissues - where adaptive immune responses initiated and lymphocytes maintained - lymphocytes are activated + maintained in the secondary tissues
Where are these secondary lymphoid tissues found?
- Lymph nodes - Located all-over but specifically at sites of potential infection – drain mucosal sites
- Spleen
-
Mucosa-associated lymphoid tissue (MALT)
- Peyer’s patches (Gut)
- Tonsils
- Appendix
- BALT – Bronchus (lungs)
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/748/439/a_image_thumb.png?1618406657)
How are immune cells circulated through the body?
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Role of the primary lymphnoid organs?
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Outline the development of T-cells from the bone marrow to their presence in secondary lymphoid tissues
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Outline the cellular organisation of the thymus
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Cellular organization of the thymus
Bi-lobed organ, lying over heart and major blood vessels
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What is the trend in T-cell production as we age?
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What does Cluster of Differentiation (CD) refer to? What is it used for?
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Outline the first stage of development/maturation of T-cells in the thymus, whereby T-cells form ‘double-negative’ thymocytes.
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After creating double negative t-cells in the thymus, how do we end up with mature t-cells?
Research how we go from double negative to double positive
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Where in the thymus do we get positive and negative selection of thymocytes? Why are these processes important?
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How is +ive selection in the thymus thought to happen?
CD8 or CD4 selection?
Instructive model, signals received through CD4 shut off the CD8 gene and cause the cell to differentiate into a Th, while signals received through CD8 shut off CD4 expression and induce Tc differentiation. According to the instructive model, the cell could go equally easily down either pathway and the first strong enough signal decides its fate.
Stochastic model, the cell is somehow randomly committed to becoming either a Tc or a Th before positive selection. If it gets the correct signal during positive selection, it proceeds down its predetermined pathway; if it doesn’t get signaled through the correct co-receptor, it dies.
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/753/826/a_image_thumb.png?1618410620)
How is -ive selection thought to happen in the thymus?
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Provide a general summary of T-cell maturation and differentiation in the thymus
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Once B-cells and T-cells have matured and entered circulation, where do they go?
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What is the general structure of a lymph node?
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If a dendritic cell picks up an antigen in a peripherical tissue (site of infection), what does it do next?
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How do Naive T and B lymphocytes enter into the lymph node?
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How does activation of naive lymphocytes in the lymph node occur?
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Outline the proces of B cell activation via specialised Follicular Dendritic Cells
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How do lymphocytes cirulate through the body?
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What is the structure and role of the spleen?
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Where are secondary lymphoid tissues normally found?
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What are Peyer’s patches (GALT)?
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How could you divide up a immune response in accordance to time since the begining of infection?
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What does the immediate immune response entail (0-4 hours)?
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What does the early induced response entail (4-96 hours)?
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What does the adaptive immune response (late) entail (>96 hours)?
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What key event has to take place to intiate the innate immune response?
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What are the four different mechanisms by which innate immune system detects foreign organisms?
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What makes a good PAMP (pathogen associated molecular patterns)?
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What are some bacterial PAMP examples? What PAMPs are common in gram +ive, -ive and mycobacteria?
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What fungal PAMPs are detected by the innate immune system?
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What are the two different broad categories of PPRs (pattern recognition receptors) and what role does each type play?
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What are Phagocytic receptors (PRRs) and what do they do?
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What are signalling receptors (PRRs) and what do they do?
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Provide three examples of Signalling PRR’s in animals + what type of cells usually express them?
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What is the structure of Toll-like receptors?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/757/940/a_image_thumb.png?1618413823)
What two feature characterize TLRs?
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Of TLRs 1-9, what is their localization in the cell? What are the consequences of receptor activation?
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What proteins do cell surface TLRs normally signal via?
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Role of NFκB in TLR’s downstream signalling?
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How do the innate and adaptive immune system recognize the presence of viruses?
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Role of endosomal TLRs in viral detection & response (innate immune system)?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/760/901/a_image_thumb.png?1618415846)
Outline how endosomal detection of viruses via TLRs takes place?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/761/029/a_image_thumb.png?1618415954)
Why do antiviral TLR’s depend on recognising endosomal nucleic acid?
Viruses are detected as nucleic acids in the wrong place because they’re otherwise indistinguishable from host –> create from host proteins
Futhermore, extracellular animal viruses are basically never in the form of exposed nucleic acids
So one needs to ‘catch’ the virsu when it uncoats in the endosome
Outline the activation of IRF3, in response to endosomal TLR activation
Endosomal pathways activate a second transcription factor, IRF3
IRF3 is key transcription factor in engaging the antiviral response in mammals
Endosomal (primarily) TLR activation triggers a signalling pathway that results in phosphorylation of IRF3 using TBK-1 (activated by TRIF), facilitating dimerization and nuclear localisation of IRF-3, where it drives transcription of its target genes (but not completely exclusive to endosomal pathways)
Key target is type 1 interferons (specific class of antiviral cytokines)
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What proinflammatory cytokines and chemokines are produced in response to TLR-NFκB activation?
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What is the mechanism behind controlling IL-1 expression?
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Why is the presence of cytosolic/intracellular bacteria a problem?
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How are cytosolic bacteria recognized by the host cell?
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Explain how NLRs help create the inflammasome complex and how that drives production of IL-1β and how it fits into the bigger picture of TLR/IL-1R activation?
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What are the two inputs required for IL-1 amplification?
- Extracellular signal (microbes) –> TLR, IL-1R and TNFR –> priming step producing pro-IL-1 & inactive NLRP3
- Intracellular signal (microbes, ROS production, K+ efflux) –> inflammasome activation
How does viral detection in the cytosol take place? What are the three classes of sensors?
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Outline the different segments of a RIG-I like receptor? What downstream targets does it act on?
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What are the specific viral RNA structures that are recognized?
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What effect does TNF (cytokine) have? (secreted by macrophages and DCs)
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What is the main target for Type-1 Interferon?
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What cells are responsible for the production of Ifnα, Ifnβ and Ifnλ?
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What are the consequences of Type-1 interferons?
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Why do T cells that have not recognise any antigens leave the lymph node? Are there still other sites of antigen presentation?
Lymphocytes are constantly being circulated why?
Because many of them will not get activated in their lifetime so to keep the system “unclogged” and moving there is constant circulation via the circulation and lymphatic system
Lymph node is suited for antigen presentation but if they are not activated they are simply re-circulated
How do type-1 interferons enhance expression of tumour-associated surface antigens?
Ordinary Transcriptional mechanism - drives Stat TF heterodimer into the nucleus to drive expression of tumour associated antigens
Do B cells enter the lymph nodes using the same mechanism as T cells?
Yes, same mechanism but they tend migrate to a different site in the lymph node
If a target is too big to phagocytose, what can Eosinophil and Basophils do?
Eosinophil and Basophil don’t typically perform phagocytosis - Macrophages are the professionals
But….
If the target is too big there are several mechanisms different effector mechanisms
- Eosinophil binds to foreign invader and releases the contents of their secretory granules
- Neutrophils can release extra-cellular traps
Difference between Phagocytosis and endocytosis?
Size of molecule taken up – phagocytosis is in relation to larger entities (cells) whereas endocytosis is normally associated to smaller molecules
How is heat produced as a side effect of inflammation?
Heat production due to circulatory (warmer) loss into tissues - heating up the tissue
Alternatively…
Fever - Systemic inflammatory heat production - cytokines signalling to the hypothalamus to set the body temperature higher –> heat production via brown fat cells
What happens to complement C3 after it gets activated by random hydrolysis but there is no pathogen nearby to bind to?
C3 has a short half-life if cleaved via random hydrolysis
Can neutrophils recognise 3Cb via a 3Cr receptor and clear opsonized bacteria or is it just the role of Macrophages?
Primarily Macrophage role
Do cells express all 10 TLRs at once? Does it depend on the cell type to some extent?
TLR is cell type dependant
But macrophages are critical for surveillance will express many/ if not all 10 TLRs at once
Is IL-1B mainly produced by immune cells?
Yes IL-1B receptors are widely expressed but the production is mainly confined to immune cells
What is the complement system?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/781/175/a_image_thumb.png?1618427269)
Does the complement system require antibodies to function?
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What are the names of the complement proteins in the complement system?
Complement components have a defined nomenclature, from the days when they were named as proteins from serum
C1-C9 are classical complement components
B, D, H, I are regulatory factors that also play key roles
When complement factors are cleaved, the products get a letter appended: so C3 is cleaved to C3a and C3b
Complexes are often described by putting these names together: so C3bBb is a complex of a fragment of C3 and a fragment of B
Which complement pathway is the most common in the complement system?
The “alternative” complement pathway
The most general/common complement pathway is called the alternative complement pathway - central protein in this pathway is C3
C3 is ordinarily present at high concentrations in serum
What reaction does C3 undergo at a small frequency? Outline the mechanism
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What role does C3 cleavage play in the alternate complement pathway?
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Where in the C3 protein does the thioester bond hydrolysis take place (which two residues)?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/781/987/a_image_thumb.png?1618428003)
After activation of 3C in presence of a generic bacterium, what happens?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/782/249/a_image_thumb.png?1618428208)
When we get amplification of 3CBb on the surface of a bacterium, what does this refer to (process)?
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What higher order complexes form in the alternate complement pathway?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/782/521/a_image_thumb.png?1618428466)
What are the respective functions of C5a and C5b?
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Outline the mechanism by which membrane attack complex (MAC) is formed?
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/782/702/a_image_thumb.png?1618428644)
Summarize the alternative complement pathway (all the different mini-pathways)
![](https://s3.amazonaws.com/brainscape-prod/system/cm/342/782/779/a_image_thumb.png?1618428738)
What is the classical complement pathway?
The “classical” complement pathway: a role for antibody
The “alternative” pathway (initiated by spontaneous C3 hydrolysis) drives 80-90% of successful complement activation
The “classical” pathway affords a mechanism for complement to be activated by specific antibodies it helps to recruit complement to the bacteria
- Explains why previous exposure to bacteria increases the efficiency of the mechanism
- An example of adaptive immunity using innate immune mechanisms to promote microbial killing – Recurring theme the adaptive immune system uses innate mechanism as an effector to kill foreign invaders